2021/10/20 更新

写真a

カミヤ ヨシノリ
紙谷 義孝
KAMIYA Yoshinori
所属
教育研究院 医歯学系 医学系列 准教授
医歯学総合研究科 生体機能調節医学専攻 器官制御医学 准教授
職名
准教授
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外部リンク

学位

  • 医学博士 ( 2001年3月   横浜市立大学 )

研究キーワード

  • 神経薬理学

  • 神経生理学

  • Anesthesiology

  • 麻酔科学

  • Neuropharmacology

  • Neurophysiology

  • Pain medicine

研究分野

  • ライフサイエンス / 麻酔科学

  • ライフサイエンス / 生理学

  • ライフサイエンス / 薬理学

  • ライフサイエンス / 医療薬学

経歴(researchmap)

  • 新潟大学大学院医歯学総合研究科   麻酔科学分野   准教授

    2017年4月 - 現在

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  • 新潟大学 医歯学総合病院 魚沼地域医療教育センター   麻酔科   麻酔科部長

    2015年4月 - 2017年3月

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  • 新潟大学 医歯学総合病院   麻酔科   講師

    2013年1月 - 2015年3月

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  • 横浜市立大学 大学院医学研究科   神経解剖学教室   助教

    2010年4月 - 2012年12月

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  • 横浜市立大学大学院医学研究科   生体制御・麻酔科学   助教

    2006年4月 - 2010年3月

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  • 横浜市立大学附属病院   麻酔科   助手

    2004年4月 - 2006年3月

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  • 横浜市立大学大学院医学研究科   生体制御・麻酔科学   博士研究員

    2002年10月 - 2004年3月

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  • セントジュード小児研究病院   発達神経生物部   博士研究員

    2000年6月 - 2002年9月

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  • 茅ヶ崎市立病院   麻酔科   後期レジデント

    1996年4月 - 1997年3月

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  • 横浜市立大学附属病院   初期研修医

    1994年5月 - 1996年3月

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  • プロフィール参照

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経歴

  • 新潟大学   医歯学総合研究科 生体機能調節医学専攻 器官制御医学   准教授

    2017年7月 - 現在

  • 新潟大学   医歯学総合病院 麻酔科   准教授

    2017年4月 - 2017年6月

  • 新潟大学   医歯学総合病院 魚沼地域医療教育センター   特任教授

    2014年10月 - 2017年3月

  • 新潟大学   医歯学総合研究科 医科学専攻   講師

    2013年1月 - 2014年9月

  • 新潟大学   医歯学総合病院 麻酔科   講師

    2013年1月 - 2014年9月

  • 新潟大学   医歯学総合研究科 生体機能調節医学専攻   講師

    2013年1月 - 2014年9月

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学歴

  • 横浜市立大学   大学院医学研究科   生体制御・麻酔科学

    1997年4月 - 2001年3月

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    国名: 日本国

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  • 横浜市立大学

    - 2001年

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  • 横浜市立大学   医学部   医学科

    1988年4月 - 1994年3月

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    国名: 日本国

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  • 横浜市立大学

    - 1994年

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所属学協会

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論文

  • Low-dose Droperidol Reduces the Amplitude of Transcranial Electrical Motor-evoked Potential: A Randomized, Double-blind, Placebo-controlled Trial. 国際誌

    Yusuke Mitsuma, Kenta Furutani, Hiroyuki Deguchi, Yoshinori Kamiya, Takahiro Tanaka, Nobutaka Kitamura, Hiroshi Baba

    Journal of neurosurgical anesthesiology   2021年8月

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    記述言語:英語   掲載種別:研究論文(学術雑誌)  

    BACKGROUND: Low-dose droperidol has been reported to suppress the amplitude of transcranial electrical motor-evoked potentials (TCE-MEPs), but no randomized controlled trials have been conducted to assess this. This randomized, double-blinded, placebo-controlled trial aimed to test the hypothesis that low-dose droperidol reduced TCE-MEP amplitudes. METHODS: Twenty female patients with adolescent idiopathic scoliosis, aged between 12 and 20 years, and scheduled to undergo corrective surgery were randomly allocated to receive droperidol (20 µg/kg) or 0.9% saline. After recording baseline TCE-MEPs, the test drug was administered, following which TCE-MEP recordings were carried out every 2 minutes for up to 10 minutes. The primary outcome was the minimum relative TCE-MEP amplitude (peak-to-peak amplitude, percentage of baseline value) recorded in the left tibialis anterior muscle. Secondary outcomes included minimum relative MEP amplitudes recorded from all other muscle groups monitored in the study. Data are expressed as medians (interquartile range). RESULTS: The TCE-MEP amplitude of the left tibialis anterior muscle was significantly reduced following droperidol administration compared with saline (37% [30% to 55%] vs. 76% [58% to 93%], respectively, P<0.01). In the other muscles, the amplitudes were reduced in the droperidol group, except for the bilateral abductor pollicis brevis and the left quadriceps femoris muscles. The relative amplitude of the bilateral F waves recorded from the gastrocnemius was decreased in the droperidol group. CONCLUSIONS: Low-dose droperidol (20 µg/kg) reduced TCE-MEP amplitudes. Anesthesiologists should pay attention to the timing of droperidol administration during intraoperative TCE-MEP recordings, even if used in a low dose.

    DOI: 10.1097/ANA.0000000000000784

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  • Distance of Catheter Tip Dislocation in Continuous Interscalene Brachial Plexus Block. 国際誌

    Tatsuya Abe, Takashi Fujiwara, Yoshinori Kamiya

    Korean journal of anesthesiology   2021年7月

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    記述言語:英語   掲載種別:研究論文(学術雑誌)  

    DOI: 10.4097/kja.21227

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  • A Bolus Dose of Ketamine Reduces the Amplitude of the Transcranial Electrical Motor-evoked Potential: A Randomized, Double-blinded, Placebo-controlled Study. 国際誌

    Kenta Furutani, Hiroyuki Deguchi, Mari Matsuhashi, Yusuke Mitsuma, Yoshinori Kamiya, Hiroshi Baba

    Journal of neurosurgical anesthesiology   33 ( 3 )   230 - 238   2021年7月

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    記述言語:英語   掲載種別:研究論文(学術雑誌)  

    BACKGROUND: A low-dose bolus or infusion of ketamine does not affect transcranial electrical motor-evoked potential (MEP) amplitude, but a dose ≥1 mg/kg may reduce MEP amplitude. We conducted a randomized, double-blinded, placebo-controlled study to evaluate the effect of ketamine (1 mg/kg) on transcranial electrical MEP. METHODS: Twenty female patients (aged 12 to 18 y) with adolescent idiopathic scoliosis scheduled to undergo posterior spinal fusion were randomly allocated to receive ketamine or saline. General anesthesia was induced and maintained with continuous infusions of propofol and remifentanil. MEP was elicited by supramaximal transcranial electrical stimulation. MEP recordings were obtained at baseline and then at 2, 4, 6, 8, and 10 minutes after administration of ketamine (1 mg/kg) or saline (0.1 ml/kg). The primary endpoint was the minimum relative MEP amplitude (peak-to-peak amplitude, % of baseline value) recorded from the left tibialis anterior muscle. The baseline amplitude recorded before test drug administration was defined as 100%. RESULTS: Medians (interquartile range) minimum MEP amplitudes in the left tibialis anterior muscle in the ketamine and saline groups were 26% (9% to 34%) and 87% (55% to 103%) of the baseline value, respectively (P<0.001). MEP amplitudes in other muscles were significantly reduced by ketamine. The suppressive effect of ketamine lasted for at least 10 minutes in each muscle. CONCLUSION: A 1-mg/kg bolus dose of ketamine can reduce MEP amplitude. Anesthesiologists should consider the dosage and timing of intravenous ketamine administration during MEP monitoring.

    DOI: 10.1097/ANA.0000000000000653

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  • Propofol reduces the amplitude of transcranial electrical motor-evoked potential without affecting spinal motor neurons: a prospective, single-arm, interventional study.

    Hiroyuki Deguchi, Kenta Furutani, Yusuke Mitsuma, Yoshinori Kamiya, Hiroshi Baba

    Journal of anesthesia   35 ( 3 )   434 - 441   2021年6月

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    記述言語:英語   掲載種別:研究論文(学術雑誌)  

    PURPOSE: Propofol inhibits the amplitudes of transcranial electrical motor-evoked potentials (TCE-MEP) in a dose-dependent manner. However, the mechanisms of this effect remain unknown. Hence, we investigated the spinal mechanisms of the inhibitory effect of propofol on TCE-MEP amplitudes by evaluating evoked electromyograms (H-reflex and F-wave) under general anesthesia. METHODS: We conducted a prospective, single-arm, interventional study including 15 patients scheduled for spine surgery under general anesthesia. Evoked electromyograms of the soleus muscle and TCE-MEPs were measured at three propofol concentrations using target-controlled infusion (TCI: 2.0, 3.0, and 4.0 µg/mL). The primary outcome measure was the left H-reflex amplitude during TCI of 4.0- compared to 2.0-µg/mL propofol administration. RESULTS: The median [interquartile range] amplitudes of the left H-reflex were 4.71 [3.42-6.60] and 5.6 [4.17-7.46] in the 4.0- and 2.0-μg/mL TCI groups (p = 0.4, Friedman test), respectively. There were no significant differences in the amplitudes of the right H-reflex and the bilateral F-wave among these groups. However, the TCE-MEP amplitudes significantly decreased with increased propofol concentrations (p < 0.001, Friedman test). CONCLUSION: Propofol did not affect the amplitudes of the H-reflex and the F-wave, whereas TCE-MEP amplitudes were reduced at higher propofol concentrations. These results suggested that propofol can suppress the TCE-MEP amplitude by inhibiting the supraspinal motor pathways more strongly than the excitability of the motor neurons in the spinal cord.

    DOI: 10.1007/s00540-021-02927-7

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  • Serotonin Plays a Key Role in the Development of Opioid-Induced Hyperalgesia in Mice. 国際誌

    Mika Sasaki, Yoshinori Kamiya, Keiko Bamba, Takeshi Onishi, Keiichiro Matsuda, Tatsuro Kohno, Miyuki Kurabe, Kenta Furutani, Harue Yanagimura

    The journal of pain   22 ( 6 )   715 - 729   2021年6月

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    記述言語:英語   掲載種別:研究論文(学術雑誌)  

    Opioid usage for pain therapy is limited by its undesirable clinical effects, including paradoxical hyperalgesia, also known as opioid-induced hyperalgesia (OIH). However, the mechanisms associated with the development and maintenance of OIH remain unclear. Here, we investigated the effect of serotonin inhibition by the 5-HT3 receptor antagonist, ondansetron (OND), as well as serotonin deprivation via its synthesis inhibitor para-chlorophenylalanine, on mouse OIH models, with particular focus on astrocyte activation. Co-administering of OND and morphine, in combination with serotonin depletion, inhibited mechanical hyperalgesia and astrocyte activation in the spinal dorsal horn of mouse OIH models. Although previous studies have suggested that activation of astrocytes in the spinal dorsal horn is essential for the development and maintenance of OIH, herein, treatment with carbenoxolone (CBX), a gap junction inhibitor that suppresses astrocyte activation, did not ameliorate mechanical hyperalgesia in mouse OIH models. These results indicate that serotonin in the spinal dorsal horn, and activation of the 5-HT3 receptor play essential roles in OIH induced by chronic morphine, while astrocyte activation in the spinal dorsal horn serves as a secondary effect of OIH. Our findings further suggest that serotonergic regulation in the spinal dorsal horn may be a therapeutic target of OIH. PERSPECTIVE: The current study revealed that the descending serotonergic pain-facilitatory system in the spinal dorsal horn is crucial in OIH, and that activation of astrocytes is a secondary phenotype of OIH. Our study offers new therapeutic targets for OIH and may help reduce inappropriate opioid use.

    DOI: 10.1016/j.jpain.2020.12.008

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  • A mechanism of re-sedation caused by remimazolam.

    Tomohiro Yamamoto, Miyuki Kurabe, Yoshinori Kamiya

    Journal of anesthesia   35 ( 3 )   467 - 468   2021年6月

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  • Epidural Administration of Ropivacaine Reduces the Amplitude of Transcranial Electrical Motor-Evoked Potentials: A Double-Blinded, Randomized, Controlled Trial. 国際誌

    Kenta Furutani, Toshiyuki Tobita, Hideaki Ishii, Hiroyuki Deguchi, Yusuke Mitsuma, Yoshinori Kamiya, Hiroshi Baba

    Anesthesia and analgesia   132 ( 4 )   1092 - 1100   2021年4月

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    記述言語:英語   掲載種別:研究論文(学術雑誌)  

    BACKGROUND: An epidurally administered local anesthetic acts primarily on the epidural nerve roots and can act directly on the spinal cord through the dural sleeve. We hypothesized that epidurally administered ropivacaine would reduce the amplitude of transcranial electrical motor-evoked potentials by blocking nerve conduction in the spinal cord. Therefore, we conducted a double-blind, randomized, controlled trial. METHODS: Thirty adult patients who underwent lung surgery were randomly allocated to 1 of 3 groups, based on the ropivacaine concentration: the 0.2% group, the 0.375% group, and the 0.75% group. The attending anesthesiologists, neurophysiologists, and patients were blinded to the allocation. The epidural catheter was inserted at the T5-6 or T6-7 interspace by a paramedian approach, using the loss of resistance technique with normal saline. General anesthesia was induced and maintained using propofol and remifentanil. Transcranial electrical motor-evoked potentials were elicited by a train of 5 pulses with an interstimulus interval of 2 milliseconds by using a constant-voltage stimulator and were recorded from the tibialis anterior muscle. Somatosensory-evoked potentials (SSEPs) were evoked by electrical tibial nerve stimulation at the popliteal fossa. After measuring the baseline values of these evoked potentials, 10 mL of epidural ropivacaine was administered at the 0.2%, 0.375%, or 0.75% concentration. The baseline amplitudes and latencies recorded before administering ropivacaine were defined as 100%. Our primary end point was the relative amplitude of the motor-evoked potentials at 60 minutes after the epidural administration of ropivacaine. We analyzed the amplitudes and latencies of these evoked potentials by using the Kruskal-Wallis test and used the Dunn multiple comparison test as the post hoc test for statistical analysis. RESULTS: The data are expressed as the median (interquartile range). Sixty minutes after epidurally administering ropivacaine, the motor-evoked potential amplitude was lower in the 0.75% group (7% [3%-18%], between-group difference P < .001) and in the 0.375% group (52% [43%-59%]) compared to that in the 0.2% group (96% [89%-105%]). The latency of SSEP was longer in the 0.75% group compared to that in the 0.2% group, but the amplitude was unaffected. CONCLUSIONS: Epidurally administered high-dose ropivacaine lowered the amplitude of motor-evoked potentials and prolonged the onset latencies of motor-evoked potentials and SSEPs compared to those in the low-dose group. High-dose ropivacaine can act on the motor pathway through the dura mater.

    DOI: 10.1213/ANE.0000000000005236

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  • Re-sleeping after reversal of remimazolam by flumazenil.

    Tomohiro Yamamoto, Miyuki Kurabe, Yoshinori Kamiya

    Journal of anesthesia   35 ( 2 )   322 - 322   2021年4月

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  • Low-dose droperidol suppresses transcranial electrical motor-evoked potential amplitude: a retrospective study. 国際誌

    Hiroyuki Deguchi, Kenta Furutani, Yusuke Mitsuma, Yoshinori Kamiya, Hiroshi Baba

    Journal of clinical monitoring and computing   35 ( 1 )   175 - 181   2021年2月

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    記述言語:英語   掲載種別:研究論文(学術雑誌)  

    Low-dose droperidol has been widely used as an antiemetic during and after surgery. Although high-dose droperidol affects motor-evoked potential, the effects of low-dose droperidol on motor-evoked potential amplitude are unclear. The aim of this study was to investigate whether low-dose droperidol affects motor-evoked potential amplitude. We retrospectively reviewed the data of patients who underwent spine surgery under general anesthesia with motor-evoked potential monitoring from February 2016 to 2017. The outcome was the motor-evoked potential amplitude of the bilateral abductor pollicis brevis muscle, tibialis anterior muscle, and abductor hallucis muscle within 1 and 1-2 h after droperidol administration, compared with the baseline motor-evoked potential value. Thirty-four patients were analyzed. The median dose of droperidol was 21 µg/kg. The motor-evoked potential amplitudes of all muscles were significantly reduced after droperidol administration and recovered to baseline values within 2 h. The reduction of all motor-evoked potential amplitudes after droperidol administration was 37-45% of baseline values. There were no significant differences in other drugs administered. There were no serious adverse effects of droperidol administration. Motor-evoked potential amplitude was suppressed by low-dose droperidol. During intraoperative motor-evoked potential monitoring in spine surgery, anesthesiologists should pay careful attention to the timing of administration of droperidol, even at low doses. Based on the results of this study, we are conducting a randomized controlled trial.

    DOI: 10.1007/s10877-020-00464-4

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  • SUZYTM forceps facilitate nasogastric tube insertion under McGRATHTM MAC videolaryngoscopic guidance: A randomized, controlled trial. 国際誌

    Kenta Furutani, Tatsunori Watanabe, Keiichiro Matsuda, Yoshinori Kamiya, Hiroshi Baba

    Medicine   99 ( 41 )   e22545   2020年10月

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    記述言語:英語   掲載種別:研究論文(学術雑誌)  

    BACKGROUND: Nasogastric tubes can be easily inserted in patients under general anesthesia. However, for difficult cases, insertion techniques that can be used in routine clinical practice are limited. SUZY forceps are designed for the removal of pharyngolaryngeal foreign bodies under guidance of a McGrath videolaryngoscope. We hypothesized that using SUZY forceps under McGrath videolaryngoscopic guidance may facilitate nasogastric tube insertion and tested this in a randomized controlled trial. METHODS: Adult patients who underwent gastrointestinal or hepato-pancreato-biliary surgery were randomly allocated to 2 groups; the SUZY group and the Magill group. Patients, nurses, and all clinical staff except for the attending anesthesiologist were blinded to group assignment throughout the study. After anesthesia induction, insertion of the nasogastric tube was performed by skilled anesthesiologists with either SUZY or Magill forceps according to group allocation under McGrath videolaryngoscopic guidance. The primary endpoint was insertion time which was defined as the time required to advance the nasogastric tube by 55 cm from the nostril. Secondary endpoints were the success rates of the nasogastric tube insertion, which were defined as a 55-cm advancement from the nostril at the 1st, 2nd, and 3rd attempt, proper insertion rate, the severity of pharyngolaryngeal complications, and hemodynamic parameters during nasogastric tube insertion. RESULTS: Sixty patients were randomized and none of these patients were excluded from the final analysis. The median [interquartile range] insertion time was 25 [18-33] seconds in the SUZY group, and 33 [21-54] seconds in the Magill group (P = .02). Success rates were not different between the groups (97% and 80% in the SUZY and Magill group at 1st attempt, respectively, P = .10). Both, the severity score of the mucosal injury and the severity of sore throat were higher in the Magill than in the SUZY group, whereas the degree of hoarseness did not differ between the 2 groups. Hemodynamic parameters were not significantly different between the groups. CONCLUSION: Using SUZY forceps under McGrath videolaryngoscopic guidance reduced the time required to insert a nasogastric tube and the severity of pharyngolaryngeal complications, when compared to using Magill forceps.

    DOI: 10.1097/MD.0000000000022545

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  • A Bolus Dose of Ketamine Reduces the Amplitude of the Transcranial Electrical Motor-evoked Potential: A Randomized, Double-blinded, Placebo-controlled Study. 査読 国際誌

    Kenta Furutani, Hiroyuki Deguchi, Mari Matsuhashi, Yusuke Mitsuma, Yoshinori Kamiya, Hiroshi Baba

    Journal of neurosurgical anesthesiology   2019年10月

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    記述言語:英語   掲載種別:研究論文(学術雑誌)  

    BACKGROUND: A low-dose bolus or infusion of ketamine does not affect transcranial electrical motor-evoked potential (MEP) amplitude, but a dose ≥1 mg/kg may reduce MEP amplitude. We conducted a randomized, double-blinded, placebo-controlled study to evaluate the effect of ketamine (1 mg/kg) on transcranial electrical MEP. METHODS: Twenty female patients (aged 12 to 18 y) with adolescent idiopathic scoliosis scheduled to undergo posterior spinal fusion were randomly allocated to receive ketamine or saline. General anesthesia was induced and maintained with continuous infusions of propofol and remifentanil. MEP was elicited by supramaximal transcranial electrical stimulation. MEP recordings were obtained at baseline and then at 2, 4, 6, 8, and 10 minutes after administration of ketamine (1 mg/kg) or saline (0.1 ml/kg). The primary endpoint was the minimum relative MEP amplitude (peak-to-peak amplitude, % of baseline value) recorded from the left tibialis anterior muscle. The baseline amplitude recorded before test drug administration was defined as 100%. RESULTS: Medians (interquartile range) minimum MEP amplitudes in the left tibialis anterior muscle in the ketamine and saline groups were 26% (9% to 34%) and 87% (55% to 103%) of the baseline value, respectively (P<0.001). MEP amplitudes in other muscles were significantly reduced by ketamine. The suppressive effect of ketamine lasted for at least 10 minutes in each muscle. CONCLUSION: A 1-mg/kg bolus dose of ketamine can reduce MEP amplitude. Anesthesiologists should consider the dosage and timing of intravenous ketamine administration during MEP monitoring.

    DOI: 10.1097/ANA.0000000000000653

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  • Acute spatial spread of NO-mediated potentiation during hindpaw ischaemia in mice. 査読

    Onishi T, Watanabe T, Sasaki M, Kamiya Y, Horie M, Tsukano H, Hishida R, Kohno T, Takebayashi H, Baba H, Shibuki K

    The Journal of Physiology   597 ( 13 )   3441 - 3455   2019年5月

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    記述言語:英語   掲載種別:学位論文(博士)  

    DOI: 10.1113/JP277615

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  • Neurosteroid dehydroepiandrosterone sulphate enhances pain transmission in rat spinal dorsal horn. 査読

    Yamamoto G, Kamiya Y, Sasaki M, Ikoma M, Baba H, Kohno T

    British Journal of Anaesthesia   123 ( 2 )   e215 - e225   2019年4月

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    記述言語:英語   掲載種別:学位論文(博士)  

    DOI: 10.1016/j.bja.2019.03.026

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  • Neural block therapy for radiation enteritis: a case report. 国際誌

    Moegi Tanaka, Yoshinori Kamiya, Hiroki Shimizu, Tatsunori Watanabe, Natsuko Naito, Hiroshi Baba

    JA clinical reports   5 ( 1 )   20 - 20   2019年3月

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    記述言語:英語   掲載種別:研究論文(学術雑誌)  

    BACKGROUND: Radiation enteritis following radiotherapy targeting the abdomen occasionally causes ulcers or ileus, which can be difficult to treat and usually progressive and refractory, significantly degrading the patient's quality of life. CASE PRESENTATION: A 58-year-old woman had undergone surgery for cervical cancer approximately 21 years ago. During treatment, she had also received radiotherapy targeting the pelvis and stomach. She presented with complaints of vomiting and lower abdominal pain and was subsequently diagnosed with multiple gastric ulcers, enterocolitis, and paralytic ileus due to late radiation-induced sequelae. We reasoned that visceral sympathetic block would improve the abdominal symptoms; therefore, we performed a splanchnic nerve block and an inferior mesenteric artery plexus block. As predicted, these block procedures improved the symptoms. CONCLUSIONS: Radiation enteritis is an iatrogenic disease, and there is no established treatment for intractable cases. However, visceral sympathetic nerve block may show efficacy as a potential therapy for radiation enteritis-associated abdominal pain and ileus.

    DOI: 10.1186/s40981-019-0239-9

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  • Learning promotes subfield-specific synaptic diversity in hippocampal CA1 neurons 査読

    Sakimoto Y, Mizuno J, Kida H, Kamiya Y, Ono Y, Mitsushima D

    Cerebral Cortex   21   2183 - 2195   2019年1月

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    記述言語:英語   掲載種別:研究論文(学術雑誌)  

    DOI: 10.1093/cercor/bhz022

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  • Short-term fasting decreases excitatory synaptic inputs to ventromedial tuberoinfundibular dopaminergic neurons and attenuates their activity in male mice 査読

    Takafumi Kubota, Atsushi Fukushima, Hiroko Hagiwara, Yoshinori Kamiya, Miyako Furuta, Tomoyuki Miyazaki, Hitomi Fujioka, Sei-Etsu Fujiwara, Toshiya Funabashi, Tatsuo Akema

    Neuroscience Letters   671   70 - 75   2018年4月

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    記述言語:英語   掲載種別:研究論文(学術雑誌)   出版者・発行元:Elsevier Ireland Ltd  

    Tuberoinfundibular dopaminergic (TIDA) neurons in the arcuate nucleus (ARC) of the hypothalamus play a role in inhibiting prolactin (PRL) secretion from the anterior pituitary. PRL is involved in a variety of behaviors, including feeding. Consequently, we hypothesized that fasting might reduce the activity of TIDA neurons, which might alter PRL secretion. However, direct examinations of TIDA neuron activity are difficult. Recently, transgenic mice were generated that expressed green fluorescent protein (GFP) under the control of the rat tyrosine hydroxylase gene. We first determined that GFP in the dorsomedial ARC was a reliable marker of TIDA neurons. Then, we performed electrophysiology and immunocytochemistry in GFP-labeled TIDA neurons to examine whether different feeding conditions could change their activity. Eight-week-old male mice were fed or fasted for 24 h. After sacrifice, we prepared acutely isolated brain slices for conducting whole-cell voltage-clamp recordings. TIDA neurons were identified with fluorescence microscopy. The mean amplitude of miniature excitatory postsynaptic currents (mEPSCs) was significantly reduced in fasting mice compared to fed mice, but different feeding conditions did not affect the mean mEPSC intervals. This result suggested that fasting reduced the number of excitatory synaptic inputs to TIDA neurons. To determine whether a reduction in excitatory synaptic inputs would cause a reduction in TIDA neuron activity, we examined the effect of 24-h fasting on c-Fos expression in the ARC. We found that fasting significantly reduced the number of Fos-positive TIDA neurons. In addition, serum PRL levels were significantly increased. Taken together, the present findings suggested that short-term fasting attenuated TIDA neuron activity.

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  • Impact of pectoral nerve block on postoperative pain and quality of recovery in patients undergoing breast cancer surgery: A randomised controlled trial 査読

    Yoshinori Kamiya, Miki Hasegawa, Takayuki Yoshida, Misako Takamatsu, Yu Koyama

    European Journal of Anaesthesiology   35 ( 3 )   215 - 223   2018年3月

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    記述言語:英語   掲載種別:研究論文(学術雑誌)   出版者・発行元:Lippincott Williams and Wilkins  

    BACKGROUND In recent years, thoracic wall nerve blocks, such as the pectoral nerve (PECS) block and the serratus plane block have become popular for peri-operative pain control in patients undergoing breast cancer surgery. The effect of PECS block on quality of recovery (QoR) after breast cancer surgery has not been evaluated. OBJECTIVES To evaluate the ability of PECS block to decrease postoperative pain and anaesthesia and analgesia requirements and to improve postoperative QoR in patients undergoing breast cancer surgery. DESIGN Randomised controlled study. SETTING A tertiary hospital. PATIENTS Sixty women undergoing breast cancer surgery between April 2014 and February 2015. INTERVENTIONS The patients were randomised to receive a PECS block consisting of 30 ml of levobupivacaine 0.25% after induction of anaesthesia (PECS group) or a saline mock block (control group). The patients answered a 40-item QoR questionnaire (QoR-40) before and 1 day after breast cancer surgery. MAIN OUTCOME MEASURES Numeric Rating Scale score for postoperative pain, requirement for intra-operative propofol and remifentanil, and QoR-40 score on postoperative day 1. RESULTS PECS block combined with propofol-remifentanil anaesthesia significantly improved the median [interquartile range] pain score at 6 h postoperatively (PECS group 1 [0 to 2] vs. Control group 1 [0.25 to 2.75]
    P=0.018]. PECSblock also reduced propofol mean (± SD) estimated target blood concentration to maintain bispectral index (BIS) between 40 and 50 (PECS group 2.65 (± 0.52) vs. Control group 3.08 (± 0.41)μgml-1
    P&lt
    0.001) but not remifentanil consumption (PECS group 10.5 (± 4.28) vs. Control group 10.4 (±4.68)μgkg-1 h-1
    P=0.95). PECS block did not improve the QoR-40 score on postoperative day 1 (PECS group 182 [176 to 189] vs. Control group 174.5 [157.75 to 175]). CONCLUSION In patients undergoing breast cancer surgery, PECS block combined with general anaesthesia reduced the requirement for propofol but not that for remifentanil, due to the inability of the PECS block to reach the internal mammary area. Further, PECS block improved postoperative pain but not the postoperative QoR-40 score due to the factors that cannot be measured by analgesia immediately after surgery, such as rebound pain.

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  • Free radical scavenger edaravone produces robust neuroprotection in a rat model of spinal cord injury. 査読 国際誌

    Hideaki Ishii, Andrey B Petrenko, Mika Sasaki, Yukio Satoh, Yoshinori Kamiya, Toshiyuki Tobita, Kenta Furutani, Mari Matsuhashi, Tatsuro Kohno, Hiroshi Baba

    Brain research   1682   24 - 35   2018年3月

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    記述言語:英語   掲載種別:研究論文(学術雑誌)  

    We used a multimodal approach to evaluate the effects of edaravone in a rat model of spinal cord injury (SCI). SCI was induced by extradural compression of thoracic spinal cord. In experiment 1, 30 min prior to compression, rats received a 3 mg/kg intravenous bolus of edaravone followed by a maintenance infusion of 1 (low-dose), 3 (moderate-dose), or 10 (high-dose) mg/kg/h edaravone. Although both moderate- and high-dose edaravone regimens promoted recovery of spinal motor-evoked potentials (MEPs) at 2 h post-SCI, the effect of the moderate dose was more pronounced. In experiment 2, moderate-dose edaravone was administered 30 min prior to compression, at the start of compression, or 10 min after decompression. Although both preemptive and coincident administration resulted in significantly improved spinal MEPs at 2 h post-SCI, the effect of preemptive administration was more pronounced. A moderate dose of edaravone resulted in significant attenuation of lipid peroxidation, as evidenced by lower concentrations of the free radical malonyldialdehyde in the spinal cord 3 h post-SCI. Malonyldialdehyde levels in the high-dose edaravone group were not reduced. Both moderate- and high-dose edaravone resulted in significant functional improvements, evidenced by better Basso-Beattie-Bresnahan (BBB) scores and better performance on an inclined plane during an 8 week period post-SCI. Both moderate- and high-dose edaravone significantly attenuated neuronal loss in the spinal cord at 8 weeks post-SCI, as evidenced by quantitative immunohistochemical analysis of NeuN-positive cells. In conclusion, early administration of a moderate dose of edaravone minimized the negative consequences of SCI and facilitated functional recovery.

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  • Comparison of a curved forceps with a conventional straight forceps for nasogastric tube insertion under videolaryngoscopic guidance A randomized, crossover manikin study 査読

    Kenta Furutani, Tatsunori Watanabe, Yoshinori Kamiya, Hiroshi Baba

    MEDICINE   96 ( 35 )   e7983   2017年9月

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    記述言語:英語   掲載種別:研究論文(学術雑誌)   出版者・発行元:LIPPINCOTT WILLIAMS & WILKINS  

    Background: Nasogastric tube (NGT) insertion is an easy procedure that can be routinely performed under general : anesthesia. However, for difficult cases, there are limited insertion techniques available in routine clinical practice, considering the flexibility of NGTs. The SUZY curved forceps are designed for the removal of pharyngolaryngeal foreign bodies under guidance of the McGRATH MAC (McG) videolaryngoscope. Because McG enables clear visualization of the esophageal inlet, we hypothesized that the SUZY forceps can facilitate easier NGT insertion compared with the conventional Magill forceps under McG guidance and designed a randomized, crossover manikin study to test this hypothesis.
    Materials and Methods: Ten anesthesiologists participated in this study. Each participant was instructed to insert an NGT using either the SUZY or the Magill forceps under McG guidance. Both types of forceps were used by each participant in a computer-generated random order. The primary outcome measure was the number of "strokes" (1 stroke was defined by a specific sequence of participant actions) required to advance the NGT 30cm from the starting point. Data are expressed as medians (interquartile ranges [ranges]).
    Results: The number of strokes required for NGT insertion was fewer in the SUZY group than in the Magill group {7 [7.0-12.5 (5-14)] vs 16.5 [13.5-20.3 (7-22)]; P &lt; .05}. The time required for NGT insertion was also lesser in the SUZY group than in the Magill group {15.4 [13.7-20.0 (7.0-38.3)] seconds vs 30.3 [22.0-42.3 (12.8-47.5) seconds]; P &lt; .05}.
    Conclusions: The SUZY curved forceps facilitated NGT insertion more effectively than the Magill straight forceps under McG guidance. Our results suggest that NGT insertion using the SUZY forceps under McG guidance is a secure and easy procedure.

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  • Acetaminophen Metabolite N-Acylphenolamine Induces Analgesia via Transient Receptor Potential Vanilloid 1 Receptors Expressed on the Primary Afferent Terminals of C-fibers in the Spinal Dorsal Horn 査読

    Nobuko Ohashi, Daisuke Uta, Mika Sasaki, Masayuki Ohashi, Yoshinori Kamiya, Tatsuro Kohno

    ANESTHESIOLOGY   127 ( 2 )   355 - 371   2017年8月

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    記述言語:英語   掲載種別:研究論文(学術雑誌)   出版者・発行元:LIPPINCOTT WILLIAMS & WILKINS  

    Background: The widely used analgesic acetaminophen is metabolized to N-acylphenolamine, which induces analgesia by acting directly on transient receptor potential vanilloid 1 or cannabinoid 1 receptors in the brain. Although these receptors are also abundant in the spinal cord, no previous studies have reported analgesic effects of acetaminophen or N-acylphenolamine mediated by the spinal cord dorsal horn. We hypothesized that clinical doses of acetaminophen induce analgesia via these spinal mechanisms.
    Methods: We assessed our hypothesis in a rat model using behavioral measures. We also used in vivo and in vitro whole cell patch-clamp recordings of dorsal horn neurons to assess excitatory synaptic transmission.
    Results: Intravenous acetaminophen decreased peripheral pinch-induced excitatory responses in the dorsal horn (53.1 +/- 20.7% of control; n = 10; P &lt; 0.01), while direct application of acetaminophen to the dorsal horn did not reduce these responses. Direct application of N-acylphenolamine decreased the amplitudes of monosynaptic excitatory postsynaptic currents evoked by C-fiber stimulation (control, 462.5 +/- 197.5 pA; N-acylphenolamine, 272.5 +/- 134.5 pA; n = 10; P = 0.022) but not those evoked by stimulation of A delta-fibers. These phenomena were mediated by transient receptor potential vanilloid 1 receptors, but not cannabinoid 1 receptors. The analgesic effects of acetaminophen and N-acylphenolamine were stronger in rats experiencing an inflammatory pain model compared to naive rats.
    Conclusions: Our results suggest that the acetaminophen metabolite N-acylphenolamine induces analgesia directly via transient receptor potential vanilloid 1 receptors expressed on central terminals of C-fibers in the spinal dorsal horn and leads to conduction block, shunt currents, and desensitization of these fibers.

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  • A functional coupling between CRMP1 and Na(v)1.7 for retrograde propagation of Semaphorin3A signaling 査読

    Masayuki Yamane, Naoya Yamashita, Tomonobu Hida, Yoshinori Kamiya, Fumio Nakamura, Pappachan Kolattukudy, Yoshio Goshima

    JOURNAL OF CELL SCIENCE   130 ( 8 )   1393 - 1403   2017年4月

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    記述言語:英語   掲載種別:研究論文(学術雑誌)   出版者・発行元:COMPANY OF BIOLOGISTS LTD  

    Semaphorin3A (Sema3A) is a secreted type of axon guidance molecule that regulates axon wiring through complexes of neuropilin-1 (NRP1) with PlexinA protein receptors. Sema3A regulates the dendritic branching through tetrodotoxin (TTX)-sensitive retrograde axonal transport of PlexA proteins and tropomyosin-related kinase A (TrkA) complex. We here demonstrate that Na(v)1.7 (encoded by SCN9A), a TTX-sensitive Na+ channel, by coupling with collapsin response mediator protein 1 (CRMP1), mediates the Sema3Ainduced retrograde transport. In mouse dorsal root ganglion (DRG) neurons, Sema3A increased co-localization of PlexA4 and TrkA in the growth cones and axons. TTX treatment and RNAi knockdown of Na(v)1.7 sustained Sema3A-induced colocalized signals of PlexA4 and TrkA in growth cones and suppressed the subsequent localization of PlexA4 and TrkA in distal axons. A similar localization phenotype was observed in crmp1(-/-) DRG neurons. Sema3A induced colocalization of CRMP1 and Na(v)1.7 in the growth cones. The half maximal voltage was increased in crmp1(-/-) neurons when compared to that in wild type. In HEK293 cells, introduction of CRMP1lowered the threshold of co-expressed exogenous Na(v)1.7. These results suggest that Na(v)1.7, by coupling with CRMP1, mediates the axonal retrograde signaling of Sema3A.

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  • Impact of pectoral nerve block on postoperative pain and quality of recovery in patients undergoing breast cancer surgery: A randomised controlled trial. 査読

    Eur J Anaesthesiol.   35 ( 3 )   215 - 223   2017年3月

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    記述言語:英語   掲載種別:研究論文(学術雑誌)  

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  • Lipid emulsion injection-induced reversal of cardiac toxicity and acceleration of emergence from general anesthesia after scalp infiltration of a local anesthetic: a case report 査読

    Hoshino R, Kamiya Y, Fujii Y, Tsubokawa T

    JA Clinical Reports   3 ( 1 )   9   2017年2月

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    記述言語:英語   掲載種別:研究論文(学術雑誌)  

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  • Bumetanide, an Inhibitor of NKCC1 (Na-K-2Cl Cotransporter Isoform 1), Enhances Propofol-Induced Loss of Righting Reflex but Not Its Immobilizing Actions in Neonatal Rats 査読

    Yukihide Koyama, Tomio Andoh, Yoshinori Kamiya, Tomoyuki Miyazaki, Koichi Maruyama, Takayuki Kariya, Takahisa Goto

    PLOS ONE   11 ( 10 )   e0164125   2016年10月

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    記述言語:英語   掲載種別:研究論文(学術雑誌)   出版者・発行元:PUBLIC LIBRARY SCIENCE  

    Gamma-aminobutyric acid (GABA) has been shown to induce excitation on immature neurons due to increased expression of Na+-K+-2Cl-co-transporter isoform 1 (NKCC1), and the transition of GABAergic signaling from excitatory to inhibitory occurs before birth in the rat spinal cord and spreads rostrally according to the developmental changes in cationchloride co-transporter expression. We previously showed that midazolam activates the hippocampal CA3 area and induces less sedation in neonatal rats compared with adolescent rats in an NKCC1-dependent manner. In the present study, we tested the hypothesis that propofol-induced loss of righting reflex (LORR) but not immobilizing actions are modulated by NKCC1-dependent mechanisms and reduced in neonatal rats compared with adolescent rats. We estimated neuronal activity in the cortex, hippocampus and thalamus after propofol administration with or without bumetanide, an NKCC1 inhibitor, by immunostaining of phosphorylated cyclic adenosine monophosphate-response element binding protein (pCREB). We studied effects of bumetanide on propofol-induced LORR and immobilizing actions in postnatal day 7 and 28 (P7 and P28) rats. The pCREB expression in the cortex (P = 0.001) and hippocampus (P = 0.01) was significantly greater in the rats receiving propofol only than in the rats receiving propofol plus bumetanide at P 7. Propofol-induced LORR or immobilizing effects did not differ significantly between P7 and P28. Bumetanide significantly enhanced propofol-induced LORR (P = 0.031) but not immobilization in P7 rats. These results are partially consistent with our hypothesis. They suggest that propofol may activate the rostral but not caudal central nervous system dependently on NKCC1, and these differential actions may underlie the different properties of sedative and immobilizing actions observed in neonatal rats.

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  • Motor Training Promotes Both Synaptic and Intrinsic Plasticity of Layer II/III Pyramidal Neurons in the Primary Motor Cortex 査読

    Hiroyuki Kida, Yasumasa Tsuda, Nana Ito, Yui Yamamoto, Yuji Owada, Yoshinori Kamiya, Dai Mitsushima

    CEREBRAL CORTEX   26 ( 8 )   3494 - 3507   2016年8月

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    記述言語:英語   掲載種別:研究論文(学術雑誌)   出版者・発行元:OXFORD UNIV PRESS INC  

    Motor skill training induces structural plasticity at dendritic spines in the primary motor cortex (M1). To further analyze both synaptic and intrinsic plasticity in the layer II/III area of M1, we subjected rats to a rotor rod test and then prepared acute brain slices. Motor skill consistently improved within 2 days of training. Voltage clamp analysis showed significantly higher alpha-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid/N-methyl-d-aspartate (AMPA/NMDA) ratios and miniature EPSC amplitudes in 1-day trained rats compared with untrained rats, suggesting increased postsynaptic AMPA receptors in the early phase of motor learning. Compared with untrained controls, 2-days trained rats showed significantly higher miniature EPSC amplitude and frequency. Paired-pulse analysis further demonstrated lower rates in 2-days trained rats, suggesting increased presynaptic glutamate release during the late phase of learning. One-day trained rats showed decreased miniature IPSC frequency and increased paired-pulse analysis of evoked IPSC, suggesting a transient decrease in presynaptic gamma-aminobutyric acid (GABA) release. Moreover, current clamp analysis revealed lower resting membrane potential, higher spike threshold, and deeper afterhyperpolarization in 1-day trained rats-while 2-days trained rats showed higher membrane potential, suggesting dynamic changes in intrinsic properties. Our present results indicate dynamic changes in glutamatergic, GABAergic, and intrinsic plasticity in M1 layer II/III neurons after the motor training.

    DOI: 10.1093/cercor/bhw134

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    その他リンク: http://orcid.org/0000-0001-9790-9867

  • Ultrasound-guided ilioinguinal/iliohypogastric block did not reduce emergence delirium after ambulatory pediatric inguinal hernia repair: a prospective randomized double-blind study 査読

    Nobuko Ohashi, Sadahei Denda, Kenta Furutani, Takayuki Yoshida, Yoshinori Kamiya, Reiko Komura, Hironobu Nishimaki, Yasushi Iinuma, Yutaka Hirayama, Shinichi Naitou, Koju Nitta, Hiroshi Baba

    SURGERY TODAY   46 ( 8 )   963 - 969   2016年8月

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    記述言語:英語   掲載種別:研究論文(学術雑誌)   出版者・発行元:SPRINGER  

    Emergence delirium (ED) is a common postoperative complication of ambulatory pediatric surgery done under general anesthesia with sevoflurane. However, perioperative analgesic techniques have been shown to reduce sevoflurane-induced ED. The primary objective of this investigation was to examine whether an ultrasound-guided ilioinguinal/iliohypogastric (II/IH) nerve block for ambulatory pediatric inguinal hernia repair could reduce the incidence of sevoflurane-induced ED.
    The subjects of this prospective randomized double-blind study were 40 boys ranging in age from 1 to 6 years, who were scheduled to undergo ambulatory inguinal hernia repair. The patients were randomized to either receive or not to receive an ultrasound-guided II/IH nerve block (Group B and Group NB, respectively). General anesthesia was maintained with sevoflurane and nitrous oxide. The primary outcome assessed was ED, evaluated using the Pediatric Anesthesia Emergence Delirium (PAED) scale 30 min after emergence from general anesthesia. The secondary outcomes assessed were postoperative pain, evaluated using the Behavioral Observational Pain Scale (BOPS), and the amount of intra-operative sevoflurane given.
    The median PAED scale scores did not differ between Groups B and NB at 30 min (P = 0.41). BOPS scores also did not differ significantly between the groups, but the mean amount of intraoperative sevoflurane given was significantly lower in Group B than in Group NB (P &lt; 0.01).
    Ultrasound-guided II/IH nerve block for ambulatory pediatric inguinal hernia repair did not reduce ED, but it did decrease the amount of intra-operative sevoflurane needed.
    Clinical Trial Registration: UMIN000008586.

    DOI: 10.1007/s00595-015-1280-6

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    その他リンク: http://orcid.org/0000-0001-9790-9867

  • パルス高周波法によるブロックが有効であった陰部神経痛の1例 査読

    清水大喜, 紙谷義孝, 鈴木博子, 渡邉美子, 馬場 洋

    日本ペインクリニック学会誌   23 ( 4 )   551 - 554   2016年

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    記述言語:日本語   掲載種別:研究論文(学術雑誌)  

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  • Thoracic paravertebral block reduced the incidence of chronic postoperative pain for more than 1 year after breast cancer surgery 査読

    Hiroki Shimizu, Yoshinori Kamiya, Hironobu Nishimaki, Sadahei Denda, Hiroshi Baba

    JA Clin Rep   1 ( 1 )   19   2015年10月

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    出版者・発行元:Springer Science $\mathplus$ Business Media  

    DOI: 10.1186/s40981-015-0023-4

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  • Pectoral nerve block combined with general anesthesia for breast cancer surgery: a retrospective comparison 査読

    Harue Morioka, Yoshinori Kamiya, Takayuki Yoshida, Hiroshi Baba

    JA Clin Rep   1 ( 1 )   15   2015年9月

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    出版者・発行元:Springer Science $\mathplus$ Business Media  

    DOI: 10.1186/s40981-015-0018-1

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  • Opioids and adjuvant drugs 査読

    Takayuki Yoshida, Yoshinori Kamiya, Tatsuro Kohno

    Neuroanesthesia and Cerebrospinal Protection   103 - 112   2015年8月

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    記述言語:英語   掲載種別:論文集(書籍)内論文   出版者・発行元:Springer Japan  

    Anesthetic agents can alter cerebral hemodynamics, which can improve or worsen intracranial conditions during surgical procedures. The effects of opioids and other adjuvant analgesics on cerebral hemodynamics are presented in this chapter. Opioids: Although reports differ, cerebral blood flow (CBF) and cerebral metabolic rate of oxygen (CMRO2) remain unaltered or are modestly increased with the administration of clinical doses of opioids, but supraclinical doses of opioids decrease both CBF and CMRO2. However, the cerebrovascular response to a change in mean arterial pressure (MAP) or arterial carbon dioxide tension is unaffected by opioids. Opioids do not increase intracranial pressure (ICP) directly. These findings suggest that clinical doses of opioids can be used safely for neuroanesthesia. The impact of opioids on an ischemic cerebrospinal injury is also discussed. Adjuvant analgesics: A substantial dose of lidocaine may decrease CMRO2. Indomethacin, but not other cyclooxygenase inhibitors, decreases CBF and ICP without decreasing MAP.

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  • Tranexamic acid evokes pain by modulating neuronal excitability in the spinal dorsal horn 査読

    Nobuko Ohashi, Mika Sasaki, Masayuki Ohashi, Yoshinori Kamiya, Hiroshi Baba, Tatsuro Kohno

    SCIENTIFIC REPORTS   5   13458   2015年8月

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    記述言語:英語   掲載種別:研究論文(学術雑誌)   出版者・発行元:NATURE PUBLISHING GROUP  

    Tranexamic acid (TXA) is an antifibrinolytic agent widely used to reduce blood loss during surgery. However, a serious adverse effect of TXA is seizure due to inhibition of gamma-aminobutyric acid (GABA) and glycine receptors in cortical neurons. These receptors are also present in the spinal cord, and antagonism of these receptors in spinal dorsal horn neurons produces pain-related phenomena, such as allodynia and hyperalgesia, in experimental animals. Moreover, some patients who are injected intrathecally with TXA develop severe back pain. However, the effect of TXA on spinal dorsal horn neurons remain poorly understood. Here, we investigated the effects of TXA by using behavioral measures in rats and found that TXA produces behaviors indicative of spontaneous pain and mechanical allodynia. We then performed whole-cell patch-clamp experiments that showed that TXA inhibits GABA(A) and glycine receptors in spinal dorsal horn neurons. Finally, we also showed that TXA facilitates activation of the extracellular signal-regulated kinase in the spinal cord. These results indicated that TXA produces pain by inhibiting GABA(A) and glycine receptors in the spinal dorsal horn.

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  • Intrathecal morphine versus epidural ropivacaine infusion for analgesia after Cesarean section: a retrospective study 査読

    Hiroko Suzuki, Yoshinori Kamiya, Takashi Fujiwara, Takayuki Yoshida, Misako Takamatsu, Kazunori Sato

    JA Clin Rep   1 ( 1 )   3   2015年8月

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    出版者・発行元:Springer Science $\mathplus$ Business Media  

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  • Spinal cord stimulation modulates supraspinal centers of the descending antinociceptive system in rats with unilateral spinal nerve injury 査読

    Toshiharu Tazawa, Yoshinori Kamiya, Ayako Kobayashi, Kensuke Saeki, Masahito Takiguchi, Yusuke Nakahashi, Hironobu Shinbori, Kengo Funakoshi, Takahisa Goto

    MOLECULAR PAIN   11 ( 1 )   36   2015年6月

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    記述言語:英語   掲載種別:研究論文(学術雑誌)   出版者・発行元:BIOMED CENTRAL LTD  

    Background: The descending antinociceptive system (DAS) is thought to play crucial roles in the antinociceptive effect of spinal cord stimulation (SCS), especially through its serotonergic pathway. The nucleus raphe magnus (NRM) in the rostral ventromedial medulla is a major source of serotonin [5-hydroxytryptamine (5-HT)] to the DAS, but the role of the dorsal raphe nucleus (DRN) in the ventral periaqueductal gray matter is still unclear. Moreover, the influence of the noradrenergic pathway is largely unknown. In this study, we evaluated the involvement of these serotonergic and noradrenergic pathways in SCS-induced antinociception by behavioral analysis of spinal nerve-ligated (SNL) rats. We also investigated immunohistochemical changes in the DRN and locus coeruleus (LC), regarded as the adrenergic center of the DAS, and expression changes of synthetic enzymes of 5-HT [tryptophan hydroxylase (TPH)] and norepinephrine [dopamine beta-hydroxylase (D beta H)] in the spinal dorsal horn.
    Results: Intrathecally administered methysergide, a 5-HT1-and 5-HT2-receptor antagonist, and idazoxan, an alpha(2)-adrenergic receptor antagonist, equally abolished the antinociceptive effect of SCS. The numbers of TPH-positive serotonergic and phosphorylated cyclic AMP response element binding protein (pCREB)-positive neurons and percentage of pCREB-positive serotonergic neurons in the DRN significantly increased after 3-h SCS. Further, the ipsilateral-to-contralateral immunoreactivity ratio of D beta H increased in the LC of SNL rats and reached the level seen in naive rats, even though the number of pCREB-positive neurons in the LC was unchanged by SNL and SCS. Moreover, 3-h SCS did not increase the expression levels of TPH and D beta H in the spinal dorsal horn.
    Conclusions: The serotonergic and noradrenergic pathways of the DAS are involved in the antinociceptive effect of SCS, but activation of the DRN might primarily be responsible for this effect, and the LC may have a smaller contribution. SCS does not potentiate the synthetic enzymes of 5HT and norepinephrine in the neuropathic spinal cord.

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  • Spinal cord stimulation modulates supraspinal centers of the descending antinociceptive system in rats with unilateral spinal nerve injury

    Toshiharu Tazawa, Yoshinori Kamiya, Ayako Kobayashi, Kensuke Saeki, Masahito Takiguchi, Yusuke Nakahashi, Hironobu Shinbori, Kengo Funakoshi, Takahisa Goto

    MOLECULAR PAIN   11   2015年6月

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    記述言語:英語   掲載種別:研究論文(学術雑誌)   出版者・発行元:BIOMED CENTRAL LTD  

    Background: The descending antinociceptive system (DAS) is thought to play crucial roles in the antinociceptive effect of spinal cord stimulation (SCS), especially through its serotonergic pathway. The nucleus raphe magnus (NRM) in the rostral ventromedial medulla is a major source of serotonin [5-hydroxytryptamine (5-HT)] to the DAS, but the role of the dorsal raphe nucleus (DRN) in the ventral periaqueductal gray matter is still unclear. Moreover, the influence of the noradrenergic pathway is largely unknown. In this study, we evaluated the involvement of these serotonergic and noradrenergic pathways in SCS-induced antinociception by behavioral analysis of spinal nerve-ligated (SNL) rats. We also investigated immunohistochemical changes in the DRN and locus coeruleus (LC), regarded as the adrenergic center of the DAS, and expression changes of synthetic enzymes of 5-HT [tryptophan hydroxylase (TPH)] and norepinephrine [dopamine beta-hydroxylase (D beta H)] in the spinal dorsal horn.
    Results: Intrathecally administered methysergide, a 5-HT1-and 5-HT2-receptor antagonist, and idazoxan, an alpha(2)-adrenergic receptor antagonist, equally abolished the antinociceptive effect of SCS. The numbers of TPH-positive serotonergic and phosphorylated cyclic AMP response element binding protein (pCREB)-positive neurons and percentage of pCREB-positive serotonergic neurons in the DRN significantly increased after 3-h SCS. Further, the ipsilateral-to-contralateral immunoreactivity ratio of D beta H increased in the LC of SNL rats and reached the level seen in naive rats, even though the number of pCREB-positive neurons in the LC was unchanged by SNL and SCS. Moreover, 3-h SCS did not increase the expression levels of TPH and D beta H in the spinal dorsal horn.
    Conclusions: The serotonergic and noradrenergic pathways of the DAS are involved in the antinociceptive effect of SCS, but activation of the DRN might primarily be responsible for this effect, and the LC may have a smaller contribution. SCS does not potentiate the synthetic enzymes of 5HT and norepinephrine in the neuropathic spinal cord.

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  • Relationship between ventral lumbar disc protrusion and contrast medium leakage during sympathetic nerve block 査読

    Toshiharu Tazawa, Yoshinori Kamiya, Mina Takamori, Ken-ichi Ogawa, Takahisa Goto

    JOURNAL OF ANESTHESIA   29 ( 1 )   138 - 142   2015年2月

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    記述言語:英語   掲載種別:研究論文(学術雑誌)   出版者・発行元:SPRINGER JAPAN KK  

    Ventral disc protrusions have been neglected because they are asymptomatic. Lumbar sympathetic nerve block (LSNB) is one of the clinical choices for refractory low back pain treatment. Leakage of the contrast medium may occur and lead to complications, especially when using a neurolytic agent. In this study, we retrospectively reviewed the magnetic resonance images (MRIs) of 52 consecutive patients with refractory low back pain due to lumbar spinal canal stenosis who underwent LSNB, and graded ventral disc protrusion at the L1/2 to L5/S1 vertebral discs on a three-point scale (grade 0 = no protrusion, grade 1 = protrusion without migration, grade 2 = protrusion with migration). We also determined if there was leakage of contrast medium in LSNB. Ventral disc protrusion was observed in all patients, and 75 % (39/52) had grade 2 protrusion in the L1/2-L3/4 vertebral discs. Moreover, the incidence of contrast medium leakage was significantly higher at the vertebrae that had grade 2 protrusion than at those with less protrusion. We revealed a higher incidence of ventral disc protrusion of the lumbar vertebrae than previously reported, and that the incidence of leakage in LSNB increased when ventral disc protrusion was present. To avoid complications, attention should be paid to ventral disc protrusions before performing LSNB.

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  • Isoflurane Impairs Learning and Hippocampal Long-term Potentiation via the Saturation of Synaptic Plasticity 査読

    Kazuhiro Uchimoto, Tomoyuki Miyazaki, Yoshinori Kamiya, Takahiro Mihara, Yukihide Koyama, Masataka Taguri, Gaku Inagawa, Takuya Takahashi, Takahisa Goto

    ANESTHESIOLOGY   121 ( 2 )   302 - 310   2014年8月

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    記述言語:英語   掲載種別:研究論文(学術雑誌)   出版者・発行元:LIPPINCOTT WILLIAMS & WILKINS  

    Background: General anesthesia induces long-lasting cognitive and learning deficits. However, the underlying mechanism remains unknown. The GluA1 subunit of AMPAR is a key molecule for learning and synaptic plasticity, which requires trafficking of GluA1-containing AMPARs into the synapse.
    Methods: Adult male rats were exposed to 1.8% isoflurane for 2 h and subjected to an inhibitory avoidance task, which is a hippocampus-dependent contextual fear learning paradigm (n = 16 to 39). The in vitro extracellular field potential of hippocampal synapses between the Schaffer collateral and the CA1 was evaluated using a multielectrode recorder (n = 6 per group). GluA1 expression in the synaptoneurosome was assessed using Western blotting (n = 5 to 8). The ubiquitination level of GluA1 was evaluated using immunoprecipitation and Western blotting (n = 7 per group).
    Results: Seven days after exposure to 1.8% isoflurane for 2 h (Iso(1.8)), the inhibitory avoidance learning (control vs. Iso(1.8); 294 +/- 34 vs. 138 +/- 28, the mean +/- SEM [%]; P = 0.002) and long-term potentiation (125.7 +/- 6.1 vs. 105.7 +/- 3.3; P &lt; 0.001) were impaired. Iso(1.8) also temporarily increased GluA1 in the synaptoneurosomes (100 +/- 9.7 vs. 138.9 +/- 8.9; P = 0.012) and reduced the GluA1 ubiquitination, a main degradation pathway of GluA1 (100 +/- 8.7 vs. 71.1 +/- 6.1; P = 0.014).
    Conclusions: Isoflurane impairs hippocampal learning and modulates synaptic plasticity in the postanesthetic period. Increased GluA1 may reduce synaptic capacity for additional GluA1-containing AMPARs trafficking.

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  • Isoflurane Impairs Learning and Hippocampal Long-term Potentiation via the Saturation of Synaptic Plasticity 査読

    Kazuhiro Uchimoto, Tomoyuki Miyazaki, Yoshinori Kamiya, Takahiro Mihara, Yukihide Koyama, Masataka Taguri, Gaku Inagawa, Takuya Takahashi, Takahisa Goto

    ANESTHESIOLOGY   121 ( 2 )   302 - 310   2014年8月

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    記述言語:英語   掲載種別:研究論文(学術雑誌)   出版者・発行元:LIPPINCOTT WILLIAMS & WILKINS  

    Background: General anesthesia induces long-lasting cognitive and learning deficits. However, the underlying mechanism remains unknown. The GluA1 subunit of AMPAR is a key molecule for learning and synaptic plasticity, which requires trafficking of GluA1-containing AMPARs into the synapse.
    Methods: Adult male rats were exposed to 1.8% isoflurane for 2 h and subjected to an inhibitory avoidance task, which is a hippocampus-dependent contextual fear learning paradigm (n = 16 to 39). The in vitro extracellular field potential of hippocampal synapses between the Schaffer collateral and the CA1 was evaluated using a multielectrode recorder (n = 6 per group). GluA1 expression in the synaptoneurosome was assessed using Western blotting (n = 5 to 8). The ubiquitination level of GluA1 was evaluated using immunoprecipitation and Western blotting (n = 7 per group).
    Results: Seven days after exposure to 1.8% isoflurane for 2 h (Iso(1.8)), the inhibitory avoidance learning (control vs. Iso(1.8); 294 +/- 34 vs. 138 +/- 28, the mean +/- SEM [%]; P = 0.002) and long-term potentiation (125.7 +/- 6.1 vs. 105.7 +/- 3.3; P &lt; 0.001) were impaired. Iso(1.8) also temporarily increased GluA1 in the synaptoneurosomes (100 +/- 9.7 vs. 138.9 +/- 8.9; P = 0.012) and reduced the GluA1 ubiquitination, a main degradation pathway of GluA1 (100 +/- 8.7 vs. 71.1 +/- 6.1; P = 0.014).
    Conclusions: Isoflurane impairs hippocampal learning and modulates synaptic plasticity in the postanesthetic period. Increased GluA1 may reduce synaptic capacity for additional GluA1-containing AMPARs trafficking.

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  • Role of nerve growth factor-tyrosine kinase receptor A signaling in paclitaxel-induced peripheral neuropathy in rats 査読

    Yusuke Nakahashi, Yoshinori Kamiya, Kengo Funakoshi, Tomoyuki Miyazaki, Kazuhiro Uchimoto, Kentaro Tojo, Kenichi Ogawa, Tetsuo Fukuoka, Takahisa Goto

    BIOCHEMICAL AND BIOPHYSICAL RESEARCH COMMUNICATIONS   444 ( 3 )   415 - 419   2014年2月

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    記述言語:英語   掲載種別:研究論文(学術雑誌)   出版者・発行元:ACADEMIC PRESS INC ELSEVIER SCIENCE  

    The mechanisms underlying paclitaxel-induced peripheral neuropathy remain unknown. Nerve growth factor (NGF) is a representative neurotrophic factor that maintains neuronal function, promotes survival, and mediates neuropathic pain. We investigated expression levels of NGF and its receptors in the dorsal root ganglia (DRG) and spinal dorsal horn (DH) following paclitaxel treatment. Intraperitoneal (I.P.) administration of paclitaxel induced significant mechanical hypersensitivity and cold allodynia in rats, significantly increased the expression of NGF and its receptor tyrosine kinase receptor A (trkA) in the DRG, and increased NGF expression in the DH. In contrast, paclitaxel treatment did not alter the mRNA levels of NGF or its receptors in the DRG, DH, sciatic nerve, or hindpaw skin. Moreover, expression of NEDD4-2, a negative regulator of trkA, was significantly increased in the DRG of paclitaxel-treated rats. Intrathecal (I.T.) administration of the tyrosine kinase receptor inhibitor k252a significantly alleviated mechanical hypersensitivity in paclitaxel-treated rats. Our results suggest that NGF-trkA signaling is involved in mechanical allodynia in paclitaxel-induced neuropathy. (C) 2014 Elsevier Inc. All rights reserved.

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  • Effects of dehydroepiandrosterone sulfate on pain transmission in the rat dorsal horn 査読

    Yamamoto G, Ikoma M, Sasaki M, Ohashi N, Kurabe M, Furutani K, Kamiya Y, Baba H

    The Journal of Functional Diagnosis of the Spinal Cord   35 ( 1 )   58 - 64   2014年

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    記述言語:日本語   掲載種別:研究論文(学術雑誌)  

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  • Intravenous administration of lidocaine inhibits excitatory synaptic transmission in spinal dorsal neurons 査読

    Kurabe M, Ohashi N, Yamamoto G, Furutani K, Ohashi M, Kamiya Y, Kohno T, Baba H

    The Journal of Functional Diagnosis of the Spinal Cord   35 ( 1 )   46 - 51   2014年

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    記述言語:日本語   掲載種別:研究論文(学術雑誌)  

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  • Effect of tranexamic acid on inhibitory synaptic transmission in spinal dorsal horn neurons 査読

    Ohashi N, Sasaki M, Yamamoto G, Kurabe M, Furutani K, Ohashi M, Kamiya Y, Kohno T, Baba H

    The Journal of Functional Diagnosis of the Spinal Cord   35 ( 1 )   52 - 57   2014年

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    記述言語:日本語   掲載種別:研究論文(学術雑誌)  

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  • Bumetanide, an Inhibitor of Cation-chloride Cotransporter Isoform 1, Inhibits γ-Aminobutyric Acidergic Excitatory Actions and Enhances Sedative Actions of Midazolam in Neonatal Rats 査読

    Yukihide Koyama, Tomio Andoh, Yoshinori Kamiya, Satoshi Morita, Tomoyuki Miyazaki, Kazuhiro Uchimoto, Takahiro Mihara, Takahisa Goto

    Anesthesiology   119 ( 5 )   1096 - 1108   2013年11月

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    記述言語:英語   掲載種別:研究論文(学術雑誌)   出版者・発行元:Ovid Technologies (Wolters Kluwer Health)  

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  • Bumetanide, an inhibitor of cation-chloride cotransporter isoform 1, inhibits γ-aminobutyric acidergic excitatory actions and enhances sedative actions of midazolam in neonatal rats. 査読

    Koyama Y, Andoh T, Kamiya Y, Morita S, Miyazaki T, Uchimoto K, Mihara T, Goto T

    Anesthesiology   119 ( 5 )   1096 - 1108   2013年11月

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    記述言語:英語   掲載種別:研究論文(学術雑誌)  

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  • Amyloid-β25–35 induces impairment of cognitive function and long-term potentiation through phosphorylation of collapsin response mediator protein 2 査読

    Toshinari Isono, Naoya Yamashita, Masami Obara, Tomomi Araki, Fumio Nakamura, Yoshinori Kamiya, Tursun Alkam, Atsumi Nitta, Toshitaka Nabeshima, Katsuhiko Mikoshiba, Toshio Ohshima, Yoshio Goshima

    Neuroscience Research   77 ( 3 )   180 - 185   2013年11月

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    記述言語:英語   掲載種別:研究論文(学術雑誌)   出版者・発行元:Elsevier {BV}  

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  • Phasic synaptic incorporation of GluR2-lacking AMPA receptors at gonadotropin-releasing hormone neurons is involved in the generation of the luteinizing hormone surge in female rats 査読

    H. Tada, Y. Kuroki, T. Funabashi, Y. Kamiya, T. Goto, K. Suyama, A. Sano, D. Mitsushima, A. M. Etgen, T. Takahashi

    Neuroscience   248   664 - 669   2013年9月

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    記述言語:英語   掲載種別:研究論文(学術雑誌)  

    Reproductive success depends on a robust and appropriately timed preovulatory luteinizing hormone (LH) surge, which is induced by the activation of gonadotropin-releasing hormone (GnRH) neurons in response to positive feedback from increasing estrogen levels. Here we document an increase in postsynaptic GluR2-lacking Ca2+-permeable AMPA-type glutamate receptors (CP-AMPARs) at synapses on GnRH neurons on the day of proestrus in rats, coincident with the increase in estrogen levels. Functional blockade of CP-AMPARs depressed the synaptic responses only on the day of proestrus and concomitantly attenuated the LH surge. Thus, the phasic synaptic incorporation of postsynaptic CP-AMPARs on GnRH neurons is involved in the generation of the LH surge. © 2013 The Authors.

    DOI: 10.1016/j.neuroscience.2013.06.040

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  • Anatomical study of superior cluneal nerve entrapment Laboratory investigation 査読

    Hiroshi Kuniya, YoicHr Aota, Tomoyuki Saito, Yoshinori Kamiya, Kengo Funakoshi, Hayato Terayama, Masahiro Itoh

    JOURNAL OF NEUROSURGERY-SPINE   19 ( 1 )   76 - 80   2013年7月

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    記述言語:英語   掲載種別:研究論文(学術雑誌)   出版者・発行元:AMER ASSOC NEUROLOGICAL SURGEONS  

    Object. Entrapment of the superior cluneal nerve (SCN) in an osteofibrous tunnel in the space surrounded by the iliac crest and the thoracolumbar fascia is a cause of low-back pain (LBP). Several anatomical and surgical reports describe SCN entrapment as a cause of LBP, and a recent clinical study reported that patients with suspected SCN disorder constitute approximately 10% of the patients suffering from LBP and/or leg symptoms. However, a detailed anatomical study of SCN entrapment is rare. The purpose of this study was to investigate the courses of SCN branches and to ascertain the frequency of SCN entrapment.
    Methods. Branches of the SCN were dissected in 109 usable specimens (54 on the right side and 55 on the left side) obtained in 59 formalin-preserved cadavers (average age at death 84.8 years old). All branches were exposed at the points where they perforated the thoracolumbar fascia. The presence or absence of an osteofibrous tunnel was ascertained and, if present, the entrapment of the branches in the tunnel was determined.
    Results. Of 109 specimens, 61(56%) had at least 1 branch running through an osteofibrous tunnel. Forty-two medial (39%), 30 intermediate (28%), and 14 lateral (13%) SCN branches passed through such a tunnel. Of these, only 2 medial branches had obvious entrapment in an osteofibrous tunnel. There were several patterns for the SCN course through the tunnel: medial branch only (n = 25), intermediate branch only (n = 11), lateral branch only (n = 4), medial and intermediate branches (n = 11), medial and lateral branches (n = 2), intermediate and lateral branches (n = 4), and all branches (n = 4).
    Conclusions. Several anatomical variations of the running patterns of SCN branches were detected. Entrapment was seen only in the medial branches. Although obvious entrapment of the SCN is rare, it may cause LBP.

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  • Anatomical study of superior cluneal nerve entrapment Laboratory investigation 査読

    Hiroshi Kuniya, YoicHr Aota, Tomoyuki Saito, Yoshinori Kamiya, Kengo Funakoshi, Hayato Terayama, Masahiro Itoh

    JOURNAL OF NEUROSURGERY-SPINE   19 ( 1 )   76 - 80   2013年7月

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    記述言語:英語   掲載種別:研究論文(学術雑誌)   出版者・発行元:AMER ASSOC NEUROLOGICAL SURGEONS  

    Object. Entrapment of the superior cluneal nerve (SCN) in an osteofibrous tunnel in the space surrounded by the iliac crest and the thoracolumbar fascia is a cause of low-back pain (LBP). Several anatomical and surgical reports describe SCN entrapment as a cause of LBP, and a recent clinical study reported that patients with suspected SCN disorder constitute approximately 10% of the patients suffering from LBP and/or leg symptoms. However, a detailed anatomical study of SCN entrapment is rare. The purpose of this study was to investigate the courses of SCN branches and to ascertain the frequency of SCN entrapment.
    Methods. Branches of the SCN were dissected in 109 usable specimens (54 on the right side and 55 on the left side) obtained in 59 formalin-preserved cadavers (average age at death 84.8 years old). All branches were exposed at the points where they perforated the thoracolumbar fascia. The presence or absence of an osteofibrous tunnel was ascertained and, if present, the entrapment of the branches in the tunnel was determined.
    Results. Of 109 specimens, 61(56%) had at least 1 branch running through an osteofibrous tunnel. Forty-two medial (39%), 30 intermediate (28%), and 14 lateral (13%) SCN branches passed through such a tunnel. Of these, only 2 medial branches had obvious entrapment in an osteofibrous tunnel. There were several patterns for the SCN course through the tunnel: medial branch only (n = 25), intermediate branch only (n = 11), lateral branch only (n = 4), medial and intermediate branches (n = 11), medial and lateral branches (n = 2), intermediate and lateral branches (n = 4), and all branches (n = 4).
    Conclusions. Several anatomical variations of the running patterns of SCN branches were detected. Entrapment was seen only in the medial branches. Although obvious entrapment of the SCN is rare, it may cause LBP.

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  • BLOOD PH IS A USEFUL INDICATOR FOR INITIATION OF THERAPEUTIC HYPOTHERMIA IN THE EARLY PHASE OF RESUSCITATION AFTER COMATOSE CARDIAC ARREST: A RETROSPECTIVE STUDY 査読

    Shunsuke Takaki, Yoshinori Kamiya, Yoshio Tahara, Masahumi Tou, Akira Shimoyama, Masayuki Iwashita

    JOURNAL OF EMERGENCY MEDICINE   45 ( 1 )   57 - 63   2013年7月

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    記述言語:英語   掲載種別:研究論文(学術雑誌)   出版者・発行元:ELSEVIER SCIENCE INC  

    Background: Therapeutic hypothermia (TH) is one of the key treatments after cardiac arrest (CA). Selection of post-CA patients for TH remains problematic, as there are no clinically validated tools to determine who might benefit from the therapy. Objective: The aim of this study was to investigate retrospectively whether laboratory findings or other patient data obtained during the early phase of hospital admission could be correlated with neurological outcome after TH in comatose survivors of CA. Methods: Medical charts of witnessed CA patients admitted between June 2003 and July 2009 who were treated with TH were reviewed retrospectively. The subjects were grouped based on their cerebral performance category (CPC) 6 months after CA, as either good recovery (GR) for CPC 1-2 or non-good recovery (non-GR) for CPC 3-5. The following well-known determinants of outcome obtained during the early phase of hospital admission were evaluated: age, gender, body mass index, cardiac origin, presence of ventricular fibrillation (VF), time from collapse to cardiopulmonary resuscitation, time from collapse to return of spontaneous circulation, body temperature, arterial blood gases, and blood test results. Results: We analyzed a total of 50 (25 GR and 25 non-GR) patients. Multivariate logistic analysis showed that initial heart rhythm and pH levels were significantly higher in the GR group than in the non-GR group (ventricular tachycardia/VF rate: p = 0.055, 95% confidence interval [CI] 0.768-84.272, odds ratio [OR] 8.047; pH: 7.155 +/- 0.139 vs. 6.895 +/- 0.100, respectively, p &lt; 0.001, 95% CI 1.838-25.827; OR 6.89). Conclusion: These results imply that in addition to initial heart rhythm, pH level may be a good candidate for neurological outcome predictor even though previous research has found no correlation between initial pH value and neurological outcome. Crown Copyright (c) 2013 Published by Elsevier Inc.

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  • Comparison of postoperative learning deficit due to isoflurane exposure or propofol infusion

    Uchimoto K, Miyazaki T, Kamiya Y, Tominaga Y, Goto T

    European Journal of Anaesthesiology   30   109 - 110   2013年6月

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    記述言語:英語   掲載種別:研究論文(その他学術会議資料等)  

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  • Effects of volatile anesthetics on the circadian rhythms of rat hippocampal acetylcholine release and locomotor activity 査読

    T. Kikuchi, H. Tan, T. Mihara, K. Uchimoto, D. Mitsushima, K. Takase, S. Morita, T. Goto, T. Andoh, Y. Kamiya

    Neuroscience   237   151 - 160   2013年5月

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    記述言語:英語   掲載種別:研究論文(学術雑誌)  

    General anesthesia is occasionally associated with postoperative complications such as sleep disorder, drowsiness, or mood alterations. Hippocampal acetylcholine (ACh), the extracellular level of which increases during the dark (active) phase and decreases during the light (rest) phase in rats, is thought to be associated with locomotor activity and be crucial for learning and memory. Propofol, an intravenous anesthetic, is known to shift the circadian rhythms of physiological parameters including locomotor activity and body temperature in both rodents and humans, while the effects of volatile anesthetics on the circadian rhythm largely remain unclear. The present study examined the effects of isoflurane anesthesia on the diurnal changes in hippocampal ACh release and locomotor activity in rats. Rats were divided into three groups: a light-phase anesthesia group (LA group), a dark-phase anesthesia group (DA group), and a control group. They were exposed to a 12-h light/12-h dark environment and anesthetized with 1.4% isoflurane for 4. h during the middle of the light phase (LA group) and dark phase (DA group). Simultaneous measurement of hippocampal ACh by microdialysis and locomotor activity were done for 60. h under free-moving conditions. Hippocampal ACh release and locomotor activity showed a clear circadian rhythm. In the DA group, but not in the LA group, the diurnal variation in ACh release was significantly disturbed and a more than 2-h phase-advance in locomotor activity was observed. There was a significant correlation between hippocampal ACh release and locomotor activity, and isoflurane anesthesia disrupted it even after anesthesia was discontinued. This study revealed that the levels and circadian rhythms of hippocampal ACh release and locomotor activity were more sensitive to isoflurane anesthesia when it was administered during the active phase. Our findings suggest that anesthesia exerts differential effects on the regulation of circadian rhythms depending on the circadian phase. © 2013 IBRO.

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    その他リンク: http://orcid.org/0000-0001-9790-9867

  • Day or Night Administration of Ketamine and Pentobarbital Differentially Affect Circadian Rhythms of Pineal Melatonin Secretion and Locomotor Activity in Rats 査読

    Takahiro Mihara, Tatsuaki Kikuchi, Yoshinori Kamiya, Motokazu Koga, Kazuhiro Uchimoto, Kiyoyasu Kurahashi, Takahisa Goto

    ANESTHESIA AND ANALGESIA   115 ( 4 )   805 - 813   2012年10月

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    記述言語:英語   掲載種別:研究論文(学術雑誌)   出版者・発行元:LIPPINCOTT WILLIAMS & WILKINS  

    BACKGROUND: Surgery with general anesthesia disturbs circadian rhythms, which may lead to postoperative sleep disorders and delirium in patients. However, it is unclear how circadian rhythms are affected by different anesthetics administered at different times during the rest-activity cycle. We hypothesized that pentobarbital (an agonist at the gamma-aminobutyric acid A receptors) and ketamine (an antagonist at the N-methyl-D-aspartate receptors) would have differential effects on circadian rhythms, and these effects would also be influenced by the time of their administration (the active versus resting phase).
    METHODS: Rats were divided into 4 groups according to the anesthetic administered (pentobarbital or ketamine) and the timing of intraperitoneal administration (active/night phase or resting/day phase). Using online pineal microdialysis, we analyzed pineal melatonin secretion and locomotor activity rhythms in rats under a light/dark (12/12-hour) cycle for 5 days after anesthesia and microdialysis catheter implantation. The data were analyzed for rhythmicity by cosinor analysis.
    RESULTS: Ketamine administered during the resting phase produced 65- and 153-minute phase advances, respectively, in melatonin secretion and locomotor activity rhythms on the first day after anesthesia. In contrast, ketamine administered during the active phase produced 43- and 235-minute phase delays. Pentobarbital had no effect on the phase of either melatonin secretion or locomotor activity, irrespective of the timing of administration. When administered during the active phase, both anesthetics decreased the amplitude of melatonin secretion on the day after anesthesia; when administered during the resting phase, however, neither anesthetic affected the amplitude. The amplitude of locomotor activity decreased in all animals for 3 days after anesthesia.
    CONCLUSION: Ketamine has opposite phase-shifting effects on circadian rhythms according to the time of administration, whereas pentobarbital has no effect. Furthermore, both anesthetics decrease the postoperative amplitude of pineal melatonin secretion if administered during the active, but not the resting, phase of the 24-hour rest-activity cycle. (Anesth Analg 2012;115:805-13)

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  • Day or Night Administration of Ketamine and Pentobarbital Differentially Affect Circadian Rhythms of Pineal Melatonin Secretion and Locomotor Activity in Rats 査読

    Takahiro Mihara, Tatsuaki Kikuchi, Yoshinori Kamiya, Motokazu Koga, Kazuhiro Uchimoto, Kiyoyasu Kurahashi, Takahisa Goto

    ANESTHESIA AND ANALGESIA   115 ( 4 )   805 - 813   2012年10月

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    記述言語:英語   掲載種別:研究論文(学術雑誌)   出版者・発行元:LIPPINCOTT WILLIAMS & WILKINS  

    BACKGROUND: Surgery with general anesthesia disturbs circadian rhythms, which may lead to postoperative sleep disorders and delirium in patients. However, it is unclear how circadian rhythms are affected by different anesthetics administered at different times during the rest-activity cycle. We hypothesized that pentobarbital (an agonist at the gamma-aminobutyric acid A receptors) and ketamine (an antagonist at the N-methyl-D-aspartate receptors) would have differential effects on circadian rhythms, and these effects would also be influenced by the time of their administration (the active versus resting phase).
    METHODS: Rats were divided into 4 groups according to the anesthetic administered (pentobarbital or ketamine) and the timing of intraperitoneal administration (active/night phase or resting/day phase). Using online pineal microdialysis, we analyzed pineal melatonin secretion and locomotor activity rhythms in rats under a light/dark (12/12-hour) cycle for 5 days after anesthesia and microdialysis catheter implantation. The data were analyzed for rhythmicity by cosinor analysis.
    RESULTS: Ketamine administered during the resting phase produced 65- and 153-minute phase advances, respectively, in melatonin secretion and locomotor activity rhythms on the first day after anesthesia. In contrast, ketamine administered during the active phase produced 43- and 235-minute phase delays. Pentobarbital had no effect on the phase of either melatonin secretion or locomotor activity, irrespective of the timing of administration. When administered during the active phase, both anesthetics decreased the amplitude of melatonin secretion on the day after anesthesia; when administered during the resting phase, however, neither anesthetic affected the amplitude. The amplitude of locomotor activity decreased in all animals for 3 days after anesthesia.
    CONCLUSION: Ketamine has opposite phase-shifting effects on circadian rhythms according to the time of administration, whereas pentobarbital has no effect. Furthermore, both anesthetics decrease the postoperative amplitude of pineal melatonin secretion if administered during the active, but not the resting, phase of the 24-hour rest-activity cycle. (Anesth Analg 2012;115:805-13)

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  • Cardiovascular intubation responses with Airway Scope and Macintosh laryngoscope reply

    Y. Koyama, M. Nishihama, G. Inagawa, Y. Kamiya, T. Miki, R. Kurihara, T. Goto

    ANAESTHESIA   67 ( 4 )   435 - 436   2012年4月

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    記述言語:英語   出版者・発行元:WILEY-BLACKWELL  

    DOI: 10.1111/j.1365-2044.2012.07071_2.x

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  • A case of ruptured cerebral aneurysm associated with coarctation of the aorta 査読

    Yuko Yonekawa, Yusuke Nakahashi, Yusuke Mizuno, Yoshinori Kamiya, Kouji Takeda, Takahisa Goto

    Japanese Journal of Anesthesiology   61 ( 3 )   326 - 328   2012年3月

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    記述言語:日本語   掲載種別:研究論文(学術雑誌)  

    A 15-year-old boy with subarachnoid hemorrhage was planned for emergency cerebral aneurysm clipping under general anesthesia. He had different blood pressure between the upper limbs and we found coarctation of the aorta at left subclavian artery bifurcation in the preoperative angiography. To prevent re-rupture of cerebral aneurysm and ischemia of abdominal organs, we monitored arterial blood pressure in bilateral radial arteries and non-invasive blood pressure in the left thigh, and his blood pressure was maintained within 120-150 mmHg of systolic pressure in the right radial artery and 50-70 mmHg of mean arterial pressure in the left radial artery and the left thigh during general anesthesia. The preoperative period elapsed uneventfully and the patient was planned for repair of coarctation of the aorta after discharge.

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  • Comparison of haemodynamic responses to tracheal intubation using the Airway Scope® and Macintosh laryngoscope in normotensive and hypertensive patients 査読

    Koyama Y, Nishihama M, Inagawa G, Kamiya Y, Miki T, Kurihara R, Goto T

    Anaesthesia   66 ( 10 )   895 - 900   2011年10月

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    記述言語:英語   掲載種別:研究論文(学術雑誌)  

    DOI: 10.1111/j.1365-2044.2011.06802.x

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  • Effects of erythropoietin on intracellular calcium concentration of rat primary cortical neurons 査読

    Tomio Andoh, Noriyuki Echigo, Yoshinori Kamiya, Michiko Hayashi, Ichidai Kudoh, Takahisa Goto

    BRAIN RESEARCH   1387   8 - 18   2011年4月

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    記述言語:英語   掲載種別:研究論文(学術雑誌)   出版者・発行元:ELSEVIER SCIENCE BV  

    Erythropoietin (Epo) has been shown to afford neuroprotection in many experimental models. Although the cytosolic Ca2+ concentration ([Ca2+)](i)) is an important factor regulating cell survival, the effects of Epo on [Ca2+](i) in neurons are not fully elucidated. We studied the effects of human recombinant Epo on [Ca2+](i) of rat primary cortical neurons in normal and excitotoxic conditions. Changes in [Ca2+](i) were measured using fura-2 microfluorometry in rat primary cortical cultures. In the control condition with 2 mM Mg2+ in the bath solution, Epo at 4 u/ml significantly increased the fluorescence ratio, but the Epo-induced increase in the fluorescence ratio was abolished by omission of Ca2+ from the bath solution and by the addition of cadmium. Omission of Mg2+ supplementation with glycine resulted in basal and periodic increases in the fluorescence ratio, due to sustained activation of N-methyl-D-asparate (NMDA) receptors. Epo at 0.4 and 4 u/ml significantly decreased the fluorescence ratio in this condition, and this effect was attenuated by the phosphoinositide 3-kinase (PI3K) inhibitors, LY 294002 and wortmannin, and the Ca-activated K channel blocker, iberiotoxin. In the presence of Mg2+ and exogenous glutamate, 4 but not 0.4 u/ml Epo slightly but significantly reduced the [Ca2+](i) elevation. These results suggest that Epo increased [Ca2+](i) in cortical neurons by inducing Ca2+ entry in the control condition but decreased [Ca2+](i) in the Mg2+-free excitotoxic condition, at least in part via PI3K-dependent activation of Ca-activated K channels. Reduction of [Ca2+](i) by Epo in the excitotoxic condition may contribute to neuroprotection. (C) 2011 Elsevier B.V. All rights reserved.

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  • Intrathecally administered Sema3A protein attenuates neuropathic pain behavior in rats with chronic constriction injury of the sciatic nerve 査読

    Michiko Hayashi, Yoshinori Kamiya, Hideki Itoh, Tomoko Higashi, Tomoyuki Miyazaki, Kengo Funakoshi, Naoya Yamashita, Yoshio Goshima, Tomio Andoh, Yoshitsugu Yamada, Takahisa Goto

    NEUROSCIENCE RESEARCH   69 ( 1 )   17 - 24   2011年1月

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    記述言語:英語   掲載種別:研究論文(学術雑誌)   出版者・発行元:ELSEVIER IRELAND LTD  

    Semaphorins, one of the repulsive axonal guidance factors during development, are produced under pathological conditions in adult animals. In the neuropathic pain state associated with peripheral nerve injury, synaptic reorganization occurs in spinal cord dorsal horn. In the present study, we investigated the roles of intrathecal administration of Sema3A, a secreted semaphorin, in the spinal cord of chronic constriction injury (CCI) model rat. Neuropilin 1 (NPR1) and Plexin A (PlexA), co-receptors of Sema3A, were expressed in the dorsal horn of naive rats. NPR1, and not PlexA, protein expression increased in the dorsal spinal cord of CCI rats. Recombinant Sema3A protein attenuated mechanical allodynia and heat hyperalgesia in CCI rats, whereas heat-inactivated Sema3A had no effect. Immunohistochemistry revealed that Sema3A partially restored the decrease of isolectin B4-positive unmyelinated nerve terminals in lamina II of the ipsilateral dorsal horn of CCI rats. Contrary to our expectations. Sema3A did not change the distribution of myelinated fibers in lamina II at 7 days after CCI. Those results suggested that the suppressive role for Sema3A in the development of neuropathic pain associated with peripheral nerve injury in adult rats, which seemed to be independent from prevention of the myelinated fiber sprouting into lamina II. (C) 2010 Elsevier Ireland Ltd and the japan Neuroscience Society. All rights reserved.

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  • A retrograde tracing study of compensatory corticospinal projections in rats with neonatal hemidecortication. 査読 国際誌

    Akira Yoshikawa, Yoshitoshi Atobe, Akihito Takeda, Yoshinori Kamiya, Masahito Takiguchi, Kengo Funakoshi

    Developmental neuroscience   33 ( 6 )   539 - 47   2011年

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    記述言語:英語   出版者・発行元:S. Karger {AG}  

    To examine the compensatory mechanisms in rats that underwent left decortication at postnatal day 7 (P7), we injected the retrograde tracers fluorescein isothiocyanate-cholera toxin B subunit (FITC-CTB) and Fast Blue (FB) into the right and left upper cervical spinal cord, respectively, at postoperative weeks 2, 3, 4, and 5 and counted the number of retrogradely labeled corticospinal neurons in the right cerebral cortex compared with that in normally developed rats. Significantly more ipsilaterally projecting neurons were labeled with FITC-CTB in the decorticated rats compared with normal rats at all time points examined. The number of labeled neurons was similar to that at P7 in normal rats. There were also some FITC-CTB and FB double-labeled neurons in both decorticated and normal rats. The number of double-labeled neurons in the decorticated rats increased each week and was significantly greater than that in normal rats at postoperative weeks 4 and 5. The present results suggest that the elimination of ipsilaterally projecting axons observed in normal rats was prevented in the decorticated rats, so that the cerebral cortex neurons on the unlesioned side projected corticospinal tracts to the ipsilateral spinal cord. Furthermore, the collaterals of the corticospinal tracts originating from the cerebral cortex on the unlesioned side also project to the ipsilateral spinal cord. These compensatory mechanisms might underlie the acquisition of motor function in these animals.

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  • Computational Analysis of the Effects of Antineoplastic Agents on Axonal Transport 査読

    Yoshio Goshima, Hiroshi Usui, Takahito Shiozawa, Tomonobu Hida, Satoshi Kuraoka, Sayumi Takeshita, Naoya Yamashita, Yasushi Ichikawa, Yoshinori Kamiya, Takahisa Gotoh, Toshiyuki Gotoh

    JOURNAL OF PHARMACOLOGICAL SCIENCES   114 ( 2 )   168 - 179   2010年10月

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    記述言語:英語   掲載種別:研究論文(学術雑誌)   出版者・発行元:JAPANESE PHARMACOLOGICAL SOC  

    Axonal transport plays a crucial role in neuronal morphogenesis, survival, and function. Despite its importance, however, the molecular mechanisms of axonal transport remain mostly unknown because a simple and quantitative assay system for axonal transport has been lacking. In order to better characterize the molecular mechanisms involved in axonal transport, we here developed a computer-assisted monitoring system. Using lipophilic fluorochrome chloromethylbenzamido dialkylcarbocyanine (CM-DiI) as a labeling dye, we have successfully labeled membranous organelles in cultured chick dorsal root ganglia neurons. We confirmed that sodium azide, an ATPase inhibitor, and nocodazole, a microtubule-destabilizing agent, markedly suppressed anterograde and retrograde axonal transport of CM-DiI labeled particles. We further tested the effects of several anti-neoplastic drugs on axonal transport. Paclitaxel, vincristine, cisplatin, and oxaliplatin, all of which are known to be neurotoxic and to cause neurological symptoms, suppressed anterograde and retrograde axonal transport. Another series of anti-neoplastic drugs, including methotrexate and 5-fluorouracil, did not affect the axonal transport. This is the first report of an automated monitoring system for axonal transport. This system will be useful for toxicity assays, characterizing axonal transport, or screening drugs that may modify neuronal functions.

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  • Computational Analysis of the Effects of Antineoplastic Agents on Axonal Transport

    Yoshio Goshima, Hiroshi Usui, Takahito Shiozawa, Tomonobu Hida, Satoshi Kuraoka, Sayumi Takeshita, Naoya Yamashita, Yasushi Ichikawa, Yoshinori Kamiya, Takahisa Gotoh, Toshiyuki Gotoh

    JOURNAL OF PHARMACOLOGICAL SCIENCES   114 ( 2 )   168 - 179   2010年10月

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    記述言語:英語   掲載種別:研究論文(学術雑誌)   出版者・発行元:JAPANESE PHARMACOLOGICAL SOC  

    Axonal transport plays a crucial role in neuronal morphogenesis, survival, and function. Despite its importance, however, the molecular mechanisms of axonal transport remain mostly unknown because a simple and quantitative assay system for axonal transport has been lacking. In order to better characterize the molecular mechanisms involved in axonal transport, we here developed a computer-assisted monitoring system. Using lipophilic fluorochrome chloromethylbenzamido dialkylcarbocyanine (CM-DiI) as a labeling dye, we have successfully labeled membranous organelles in cultured chick dorsal root ganglia neurons. We confirmed that sodium azide, an ATPase inhibitor, and nocodazole, a microtubule-destabilizing agent, markedly suppressed anterograde and retrograde axonal transport of CM-DiI labeled particles. We further tested the effects of several anti-neoplastic drugs on axonal transport. Paclitaxel, vincristine, cisplatin, and oxaliplatin, all of which are known to be neurotoxic and to cause neurological symptoms, suppressed anterograde and retrograde axonal transport. Another series of anti-neoplastic drugs, including methotrexate and 5-fluorouracil, did not affect the axonal transport. This is the first report of an automated monitoring system for axonal transport. This system will be useful for toxicity assays, characterizing axonal transport, or screening drugs that may modify neuronal functions.

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  • Skin-derived precursors differentiating into dopaminergic neuronal cells in the brains of Parkinson disease model rats Laboratory investigation 査読

    Tetsuhiro Higashida, Susumu Jitsuki, Atsuhiko Kubo, Dai Mitsushima, Yoshinori Kamiya, Hiroshi Kanno

    JOURNAL OF NEUROSURGERY   113 ( 3 )   648 - 655   2010年9月

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    記述言語:英語   掲載種別:研究論文(学術雑誌)   出版者・発行元:AMER ASSOC NEUROLOGICAL SURGEONS  

    Object. In the authors&apos; previous study. they observed that amino acids 157-171 of von Hippel-Lindau protein (VHL peptide) induced neuronal differentiation of skin-derived precursors. They also noted that transplantation of these differentiated cells into the striata of a Parkinson disease (PD) rat model reduced apomorphine-induced rotations. In the present study, they investigated if these cells produce dopamine in the striatum.
    Methods. Skin-derived precursors were differentiated into neurons using VHL peptide and transplanted into the striata of a PD model of rats. Four weeks after transplantation, a probe was inserted into rat striata and extracellular dopamine was extracted by microdialysis. Dopamine levels were measured by high-pressure liquid chromatography. Brain sections were assessed by immunohistochemical analysis for the presence of tyrosine hydroxylase and dopamine transporter.
    Results. Increased dopamine levels in the striata of the rats were observed after transplantation (p &lt; 0.01), and these were correlated with a reduction in the number of apomorphine-induced rotations (p &lt; 0.05). Skin-derived precursors observed along the tract of transplantation were positive for tyrosine hydroxylase and dopamine transporter.
    Conclusions. This study suggests that transplantation of skin-derived precursors, differentiated into neuronal cells using VHL peptide, can improve PD-like symptoms by enabling production of dopamine in the striata in a PD model of rats. (DOI: 10.3171/2010.2.JNS091432)

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  • Skin-derived precursors differentiating into dopaminergic neuronal cells in the brains of Parkinson disease model rats Laboratory investigation 査読

    Tetsuhiro Higashida, Susumu Jitsuki, Atsuhiko Kubo, Dai Mitsushima, Yoshinori Kamiya, Hiroshi Kanno

    JOURNAL OF NEUROSURGERY   113 ( 3 )   648 - 655   2010年9月

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    記述言語:英語   掲載種別:研究論文(学術雑誌)   出版者・発行元:AMER ASSOC NEUROLOGICAL SURGEONS  

    Object. In the authors&apos; previous study. they observed that amino acids 157-171 of von Hippel-Lindau protein (VHL peptide) induced neuronal differentiation of skin-derived precursors. They also noted that transplantation of these differentiated cells into the striata of a Parkinson disease (PD) rat model reduced apomorphine-induced rotations. In the present study, they investigated if these cells produce dopamine in the striatum.
    Methods. Skin-derived precursors were differentiated into neurons using VHL peptide and transplanted into the striata of a PD model of rats. Four weeks after transplantation, a probe was inserted into rat striata and extracellular dopamine was extracted by microdialysis. Dopamine levels were measured by high-pressure liquid chromatography. Brain sections were assessed by immunohistochemical analysis for the presence of tyrosine hydroxylase and dopamine transporter.
    Results. Increased dopamine levels in the striata of the rats were observed after transplantation (p &lt; 0.01), and these were correlated with a reduction in the number of apomorphine-induced rotations (p &lt; 0.05). Skin-derived precursors observed along the tract of transplantation were positive for tyrosine hydroxylase and dopamine transporter.
    Conclusions. This study suggests that transplantation of skin-derived precursors, differentiated into neuronal cells using VHL peptide, can improve PD-like symptoms by enabling production of dopamine in the striata in a PD model of rats. (DOI: 10.3171/2010.2.JNS091432)

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  • T-type Ca2+ Channels Promote Oxygenation-induced Closure of the Rat Ductus Arteriosus Not Only by Vasoconstriction but Also by Neointima Formation 査読

    Toru Akaike, Mei-Hua Jin, Utako Yokoyama, Hiroko Izumi-Nakaseko, Qibin Jiao, Shiho Iwasaki, Mari Iwamoto, Shigeru Nishimaki, Motohiko Sato, Shumpei Yokota, Yoshinori Kamiya, Satomi Adachi-Akahane, Yoshihiro Ishikawa, Susumu Minamisawa

    JOURNAL OF BIOLOGICAL CHEMISTRY   284 ( 36 )   24025 - 24034   2009年9月

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    記述言語:英語   掲載種別:研究論文(学術雑誌)   出版者・発行元:AMER SOC BIOCHEMISTRY MOLECULAR BIOLOGY INC  

    The ductus arteriosus (DA), an essential vascular shunt for fetal circulation, begins to close immediately after birth. Although Ca2+ influx through several membrane Ca2+ channels is known to regulate vasoconstriction of the DA, the role of the T-type voltage-dependent Ca2+ channel (VDCC) in DA closure remains unclear. Here we found that the expression of alpha 1G, a T-type isoform that is known to exhibit a tissue-restricted expression pattern in the rat neonatal DA, was significantly up-regulated in oxygenated rat DA tissues and smooth muscle cells (SMCs). Immunohistological analysis revealed that alpha 1G was localized predominantly in the central core of neonatal DA at birth. DA SMC migration was significantly increased by alpha 1G overexpression. Moreover, it was decreased by adding alpha 1G-specific small interfering RNAs or using R(-)-efonidipine, a highly selective T-type VDCC blocker. Furthermore, an oxygenation-mediated increase in an intracellular Ca2+ concentration of DA SMCs was significantly decreased by adding alpha 1G-specific siRNAs or using R(-)-efonidipine. Although a prostaglandin E receptor EP4 agonist potently promoted intimal thickening of the DA explants, R(-)-efonidipine (10(-6) M) significantly inhibited EP4-promoted intimal thickening by 40% using DA tissues at preterm in organ culture. Moreover, R(-)-efonidipine (10(-6) M) significantly attenuated oxygenation-induced vasoconstriction by similar to 27% using a vascular ring of fetal DA at term. Finally, R(-)-efonidipine significantly delayed the closure of in vivo DA in neonatal rats. These results indicate that T-type VDCC, especially alpha 1G, which is predominantly expressed in neonatal DA, plays a unique role in DA closure, implying that T-type VDCC is an alternative therapeutic target to regulate the patency of DA.

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  • Lidocaine Concentration in Cerebrospinal Fluid after Epidural Administration A Comparison between Epidural and Combined Spinal-Epidural Anesthesia 査読

    Yoshinori Kamiya, Tatsuaki Kikuchi, Gaku Inagawa, Hiroshi Miyazaki, Masashi Miura, Satoshi Morita, Takahisa Goto

    ANESTHESIOLOGY   110 ( 5 )   1127 - 1132   2009年5月

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    記述言語:英語   掲載種別:研究論文(学術雑誌)   出版者・発行元:LIPPINCOTT WILLIAMS & WILKINS  

    Background: In this study, lidocaine concentrations in cerebrospinal fluid (CSF) at different interspaces were measured with or without preceding spinal anesthesia, 10 min after epidural injection of lidocaine, to investigate the effects of preceding meningeal puncture on CSF concentrations of epidurally administered local anesthetic.
    Methods: Sixty patients scheduled to receive combined spinal-epidural anesthesia were randomly allocated to receive either spinal anesthesia first (group CSEA) or epidural lidocaine first (group Epi). Each group was divided into three subgroups in which the site of epidural cannulation and spinal tap were separated by one, three, or five interspaces (sets 1, H, and 111, respectively). CSF was collected from the L4-L5 interspace 10 min after 10 ml lidocaine, 1%, was administered epidurally. In group Epi, CSF was collected after epidural administration of lidocaine and before spinal anesthesia. In group CSEA, spinal anesthesia was performed at the L3-L4 interspace after epidural cannulation and epidural lidocaine was administered postoperatively, after which CSF was sampled.
    Results. Lidocaine concentrations in CSF were significantly higher with increasing proximity of epidural injection site to CSF collection site in both groups. There were no significant differences in CSF lidocaine concentrations between group CSEA and group Epi in set 1, although lidocaine concentrations were significantly higher in group CSEA set II and III patients.
    Conclusion: Lidocaine concentration in CSF was similar with or without preceding meningeal puncture beneath the epidural administration site.

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  • Lidocaine Concentration in Cerebrospinal Fluid after Epidural Administration A Comparison between Epidural and Combined Spinal-Epidural Anesthesia 査読

    Yoshinori Kamiya, Tatsuaki Kikuchi, Gaku Inagawa, Hiroshi Miyazaki, Masashi Miura, Satoshi Morita, Takahisa Goto

    ANESTHESIOLOGY   110 ( 5 )   1127 - 1132   2009年5月

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    記述言語:英語   掲載種別:研究論文(学術雑誌)   出版者・発行元:LIPPINCOTT WILLIAMS & WILKINS  

    Background: In this study, lidocaine concentrations in cerebrospinal fluid (CSF) at different interspaces were measured with or without preceding spinal anesthesia, 10 min after epidural injection of lidocaine, to investigate the effects of preceding meningeal puncture on CSF concentrations of epidurally administered local anesthetic.
    Methods: Sixty patients scheduled to receive combined spinal-epidural anesthesia were randomly allocated to receive either spinal anesthesia first (group CSEA) or epidural lidocaine first (group Epi). Each group was divided into three subgroups in which the site of epidural cannulation and spinal tap were separated by one, three, or five interspaces (sets 1, H, and 111, respectively). CSF was collected from the L4-L5 interspace 10 min after 10 ml lidocaine, 1%, was administered epidurally. In group Epi, CSF was collected after epidural administration of lidocaine and before spinal anesthesia. In group CSEA, spinal anesthesia was performed at the L3-L4 interspace after epidural cannulation and epidural lidocaine was administered postoperatively, after which CSF was sampled.
    Results. Lidocaine concentrations in CSF were significantly higher with increasing proximity of epidural injection site to CSF collection site in both groups. There were no significant differences in CSF lidocaine concentrations between group CSEA and group Epi in set 1, although lidocaine concentrations were significantly higher in group CSEA set II and III patients.
    Conclusion: Lidocaine concentration in CSF was similar with or without preceding meningeal puncture beneath the epidural administration site.

    DOI: 10.1097/ALN.0b013e31819daf15

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  • Anesthetic management of a patient with HOCM even after PTSMA 査読

    Hiroko Fujimoto, Yoshinori Kamiya, Hiroshi Ohki, Takahisa Goto

    Japanese Journal of Anesthesiology   57 ( 10 )   1276 - 1279   2008年10月

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    記述言語:日本語   掲載種別:研究論文(学術雑誌)  

    A 74-year-old woman previously treated with percutaneous transluminnal septal myocardial ablation (PTSMA) for severe hypertrophic obstructive cardiomyopathy (HOCM) underwent laparoscopic cholecystectomy under general anesthesia. The PTSMA was performed for HOCM 5 month before surgery and the left ventricular outflow pressure gradient (LVOTG) was reduced from 100 mmHg to 30 mmHg. After anesthetic induction, severe hypotension occurred concomitantly with asymmetrical septal hypertrophy (ASH) and systolic anterior movement of the mitral valve leaflet (SAM). Hypotension was treated with fluid therapy and the vasopressors (methoxamine and noradrenaline). Care should be taken for the anesthetic management of a patient with HOCM even after PTSMA.

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  • Randomized prospective study comparing the laryngeal tube suction II with the proSeal™ laryngeal mask airway in anesthetized and paralyzed patients 査読

    Kikuchi T, Kamiya Y, Ohtsuka T, Miki T, Goto T

    Anesthesiology   109 ( 1 )   54 - 60   2008年7月

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    記述言語:英語   掲載種別:研究論文(学術雑誌)  

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  • Randomized Prospective Study Comparing the Laryngeal Tube Suction II with the ProSeal™ Laryngeal Mask Airway in Anesthetized and Paralyzed Patients 査読

    Tatsuaki Kikuchi, Yoshinori Kamiya, Tsuyoshi Ohtsuka, Tomoko Miki, Takahisa Goto

    Anesthesiology   109 ( 1 )   54 - 60   2008年7月

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    記述言語:英語   掲載種別:研究論文(学術雑誌)   出版者・発行元:Ovid Technologies (Wolters Kluwer Health)  

    DOI: 10.1097/ALN.0b013e318178819b

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  • Differential effects of isoflurane on A-type and delayed rectifier K channels in rat substantia nigra 査読

    Dai Ishiwa, Isao Nagata, Tatsuo Ohtsuka, Hideki Itoh, Yoshinori Kamiya, Kenichi Ogawa, Mariko Sakai, Nagaaki Sekino, Yoshitsugu Yamada, Takahisa Goto, Tomio Andoh

    EUROPEAN JOURNAL OF PHARMACOLOGY   580 ( 1-2 )   122 - 129   2008年2月

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    記述言語:英語   掲載種別:研究論文(学術雑誌)   出版者・発行元:ELSEVIER SCIENCE BV  

    The authors previously demonstrated that isoflurane, a widely used volatile anesthetic, induced depolarization and increased the frequency of spontaneous action potentials in principal dopamine neurons in rat substantia nigra pars compacta. We studied the effects of isoflurane on voltage-dependent K channels to clarify the mechanisms of the increase in excitability in these neurons. Voltage-clamp whole-cell recordings were made in rat midbrain slices. We recorded the outward membrane currents in response to depolarizing voltage steps from -120 mV and -25 mV and isolated the transient outward current mediated through A-type K channels by subtraction. Isoflurane at clinically relevant concentrations accelerated the decay of the A-type K current and delayed the recovery from inactivation without changing the steady-state inactivation curves. Isoflurane did not affect the non-inactivating outward current. Addition of 4-aminopyridine partially occluded the excitatory effects of isoflurane in current-clamp recordings. These results demonstrate that isoflurane accelerated the inactivation and delayed the recovery from inactivation of A-type K channels in principal neurons in rat substantia nigra pars compacta without affecting delayed rectifier K channels. These effects may contribute in part to excitation of these neurons and the isoflurane-induced increases in dopamine release reported in vitro and in vivo. (C) 2007 Elsevier B.V. All rights reserved.

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  • Comparison of the Airway Scope®, gum elastic bougie and fibreoptic bronchoscope in simulated difficult tracheal intubation: A manikin study

    Y. Koyama, Gaku Inagawa, T. Miyashita, T. Kikuchi, N. Miura, T. Miki, R. Kurihara, Y. Kamiya, T. Goto

    Anaesthesia   62 ( 9 )   936 - 939   2007年9月

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    記述言語:英語   掲載種別:研究論文(学術雑誌)  

    We compared the Airway Scope® with a gum elastic bougie and fibreoptic bronchoscope in a manikin with a simulated Cormack and Lehane Grade 3 laryngoscopic view. Twenty-seven anaesthetists intubated the trachea of the manikin with these devices and the time required for intubation was measured. They were then asked to rate the subjective difficulty of intubation (1 = very easy; 5 = very difficult). Mean (SD) intubation times were 16.6 (11.2) s with the Airway Scope, 29.4 (10.9) s with the gum elastic bougie (p &lt; 0.0001), and 30.6 (20.0) s with the fibreoptic bronchoscope (p &lt; 0.0001). The median (range) difficulty was 2 (1-4) with the Airway Scope, 3 (2-4) with the gum elastic bougie (p &lt; 0.001), and 2 (1-5) with the fibreoptic bronchoscope (p = 0.014). In Cormack and Lehane grade 3 laryngoscopic views, the Airway Scope may enable faster and easier tracheal intubation than does a Macintosh laryngoscope with a gum elastic bougie or a fibreoptic bronchoscope. © 2007 The Authors Journal compilation 2007 The Association of Anaesthetists of Great Britain and Ireland.

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  • The effect of isoflurane on the oxygen radical level in primary cultures of rat cortical neurons 査読

    Echigo N, Saitou Sibakawa Y, Kamiya Y, Yamada Y, Goto T, Andoh T

    Yokohama Medical Journal   58 ( 1 )   17 - 23   2007年

  • A(1) adenosine receptor-mediated modulation of neuronal ATP-sensitive K channels in rat substantia nigra

    Tomio Andoh, Dai Ishiwa, Yoshinori Kamiya, Noriyuki Echigo, Takahisa Goto, Yoshitsugu Yamada

    BRAIN RESEARCH   1124 ( 1 )   55 - 61   2006年12月

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    記述言語:英語   掲載種別:研究論文(学術雑誌)   出版者・発行元:ELSEVIER SCIENCE BV  

    ATP-sensitive K (K-ATP) channels, widely expressed in cytoplasmic membranes of neurons, couple cell metabolism to excitability. They are considered to play important roles in controlling seizure activity during hypoxia and in neuroprotection against cell damage during hypoxia, ischemia and excitotoxicity. It is known that adenosine augments the opening of cardiac surface K-ATP channels by reducing the sensitivity of these channels to ATP blockade. We investigated whether a similar modulation occurs in neuronal channels. Whole cell voltage-clamp recordings were made using rat midbrain slices to record the membrane current and conductance in principal neurons of the substantia nigra pars compacta (SNc). When the pipette solution contained 1 mM ATP, the membrane current at -60 mV and cellular conductance remained stable for at least 15 min. When slices were treated with (-)-N-6-2-phenylisopropyl adenosine (R-PIA), a selective agonist for A, adenosine receptors, in the same condition, the outward current developed slowly to the amplitude of 109.9 +/- 26.6 pA, and conductance increased to 229 +/- 50% of the baseline. These changes were strongly inhibited by 200 mu M tolbutamide, a K-ATP channel blocker, suggesting that opening of K-ATP channels mediated these changes. Pretreatment with 8-cyclopentyltheophylline (CPT), a selective A, adenosine receptor antagonist, abolished the outward current and conductance increases. Treatment of adenosine resulted in the similar changes sensitive to tolbutamide. These changes were abolished by CPT. These results suggest that activation of A, adenosine receptors promotes the opening of K-ATP channels in principal neurons of the SNc by removing the blockade by ATP. (c) 2006 Elsevier B.V. All rights reserved.

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  • Pre-anesthetic evaluation can play a crucial role in the determination of airway management in a child with oropharyngeal tumor 査読

    Yoshihiro Aoi, Yoshinori Kamiya, Masashi Shioda, Ryosuke Furuya, Yoshitsugu Yamada

    Journal of Anesthesia   20 ( 3 )   215 - 219   2006年8月

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    記述言語:英語   掲載種別:研究論文(学術雑誌)   出版者・発行元:Springer Science $\mathplus$ Business Media  

    We experienced a case of a huge hemangioma occupying the oropharyngeal space in an 11-year-old child. Although urgent surgical tracheostomy under local anesthesia was suggested initially, medical interview and findings of computerized tomography and fiberoptic laryngoscopy revealed that the airway of the patient was relatively stable when she was in the semi-left decubitus position. General anesthetic induction would have had potential risks of airway obstruction. Thus, after placing the patient in the semi-left decubutus position, we chose semi-awake induction to secure the airway. With a small dose of fentanyl, we accomplished orotracheal intubation. In this report, we discuss the importance of referring to an airway management algorithm when encountering a difficult airway. © JSA 2006.

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  • Modulation of neuronal ATP-sensitive K channels by A1 adenosine receptor-mediated signalling in rat substantia nigra 査読

    Echigo N, Ishiwa D, Kamiya Y, Yamada Y, Andoh T

    Yokohama Medical Journal   57 ( 1-2 )   9 - 16   2006年

  • Effects of barbiturates on ATP-sensitive K channels in rat substantia nigra

    T Ohtsuka, D Ishiwa, Y Kamiya, H Itoh, Nagata, I, Y Saito, Y Yamada, M Sumitomo, T Andoh

    NEUROSCIENCE   137 ( 2 )   573 - 581   2006年

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    記述言語:英語   掲載種別:研究論文(学術雑誌)   出版者・発行元:PERGAMON-ELSEVIER SCIENCE LTD  

    ATP-sensitive K channels are widely expressed in cytoplasmic membranes of neurons, and they couple cell metabolism to excitability. They are thought to be involved in neuroprotection against cell damage during hypoxia, ischemia and excitotoxicity by hyperpolarizing neurons and reducing excitability. Although barbiturates are often used in patients with brain ischemia, the effects of these agents on neuronal ATP-sensitive K channels have not been clarified. We studied the effects of thiopental and pentobarbital on surface ATP-sensitive K channels in principal neurons of rat substantia nigra pars compacta. Whole cell voltage- and current-clamp recordings were made using rat midbrain slices. ATP-sensitive K channels were activated by intracellular dialysis with an ATP-free pipette solution during perfusion with a glucose-free solution. When the pipette solution contained 4 mM ATP and the perfusing solution contained 25 mM glucose, the membrane current at -60 mV remained stable. When intracellular ATP was depleted, hyperpolarization and an outward current developed slowly. Although thiopental did not affect the membrane current in the presence of ATP and glucose, it reversibly inhibited the hyperpolarization and outward current induced by intracellular ATP depletion at 100 and 300 mu M. Thiopental reduced the ATP depletion-induced outward current by 4.7%, 36.7% and 87% at 30, 100 and 300 mu M, respectively. The high dose of pentobarbital also exhibited similar effects on ATP-sensitive K channels. These results suggest that barbiturates at high concentrations but not at clinically relevant concentrations inhibit ATP-sensitive K channels activated by intracellular ATP depletion in rat substantia nigra. (c) 2005 Published by Elsevier Ltd on behalf of IBRO.

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  • Effects of ketamine and propofol on inflammatory responses of primary glial cell cultures stimulated with lipopolysaccharide 査読

    YS Shibakawa, Y Sasaki, Y Goshima, N Echigo, Y Kamiya, K Kurahashi, Y Yamada, T Andoh

    BRITISH JOURNAL OF ANAESTHESIA   95 ( 6 )   803 - 810   2005年12月

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    記述言語:英語   掲載種別:研究論文(学術雑誌)   出版者・発行元:OXFORD UNIV PRESS  

    Background. Ketamine has been reported to exert anti-inflammatory effects on macrophages stimulated with lipopolysaccharide (LPS) in vitro and in vivo. Several studies have reported conflicting results regarding the effects of propofol on cytokine production from immune cells. However, there have been no reports of the effects of these agents on inflammatory responses in glial cells. We investigated the effects of ketamine and propofol on LPS-induced production of nitric oxide, tumour necrosis factor-alpha (TNF-alpha) and prostaglandin E-2 (PGE(2)) from primary cultures of rat glial cells in vitro.
    Methods. Glial cells were stimulated with LPS in the absence and presence of various concentrations of ketamine (30-1000 mu M) or propofol (30 and 300 mu M). Nitric oxide released into the culture media was determined by measuring nitrite using the Griess reaction, and concentrations of TNF-alpha and PGE(2) were measured by enzyme-linked immunosorbent assay (ELISA).
    Results. Ketamine reduced LPS-induced TNF-alpha production without significant inhibition of nitrite release in mixed glial cells, astrocyte cultures and microglial cultures. Ketamine also inhibited LPS-induced production of PGE(2) in astrocyte cultures. In contrast, propofol had no effect on LPS-induced nitrite or TNF-alpha production in mixed glial cells.
    Conclusions. The data demonstrate that ketamine inhibited some of the inflammatory responses of both astrocytes and microglial cells treated with LPS without causing major change in nitric oxide release. Propofol had no effect on the production of nitric oxide or TNF-alpha from LPS-stimulated glial cells.

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  • Effects of anesthetics on ATP-sensitive K channels in rat substantia nigra 査読

    T. Andoh, T. Ohtsuka, D. Ishiwa, Y. Kamiya, Y. Yamada

    International Congress Series   1283   185 - 188   2005年11月

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    記述言語:英語   掲載種別:研究論文(学術雑誌)  

    ATP-sensitive K (KATP) channels are widely expressed in cytoplasmic membranes of neurons and they couple cell metabolism to excitability. They are known to play important roles in neuroprotection during ischemia and excitotoxicity. We studied the effects of three anesthetics on surface KATP channels in principal neurons of rat substantia nigra pars compacta. Whole cell voltage- and current-clamp recordings were made using rat midbrain slices. When neurons were dialyzed with an ATP-free pipette solution during perfusion with a glucose-free external solution, a hyperpolarization and an outward current developed slowly in a tolbutamide-inhibitable manner. Ketamine and thiopental did not affect the membrane potential or current when intracellular ATP was preserved, however, isoflurane slightly depolarized the neurons and increased frequency of spontaneous firings. The hyperpolarization and outward current induced by intracellular ATP depletion were reversibly inhibited by ketamine and thiopental at 100 and 300 μM but not by 704 μM isoflurane. These results suggest that surface KATP channels in these neurons are inhibited by high concentrations of ketamine and thiopental but not by isoflurane when the channels are activated. Our findings do not support the idea that KATP channel activation is important for previously reported neuroprotective actions of isoflurane. © 2005 Elsevier B.V. All rights reserved.

    DOI: 10.1016/j.ics.2005.07.036

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  • Roles of the N-terminal domain on the function and quaternary structure of the ionotropic glutamate receptor 査読

    S Matsuda, Y Kamiya, M Yuzaki

    JOURNAL OF BIOLOGICAL CHEMISTRY   280 ( 20 )   20021 - 20029   2005年5月

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    記述言語:英語   掲載種別:研究論文(学術雑誌)   出版者・発行元:AMER SOC BIOCHEMISTRY MOLECULAR BIOLOGY INC  

    The &alpha;-amino-3-hydroxyl-5-methyl-4-isoxazolepropionic acid (AMPA) subtype of ionotropic glutamate receptors (iGluRs) mediates fast excitatory neurotransmission in the mammalian brain. Although the most N-terminal leucine/isoleucine/valine-binding protein (LIVBP) domain is suggested to play a role in the initial assembly of iGluR subunits, it is unclear how this domain is arranged and functions in intact iGluRs. Similarly, although recent crystallographic analyses indicate that the isolated ligand-binding lysine/arginine/ornithine-binding protein domain forms a 2-fold symmetric dimer, the subunit stoichiometry of intact iGluRs remains elusive. Here, we developed a new approach to address these issues. The LIVBP domain of the GluR1 subunit of AMPA receptors was replaced by leucine-zipper peptides designed to form stable symmetric dimers, trimers, tetramers, or pentamers. All these mutant GluR1s were expressed in human embryonic kidney 293 cells and were transported to the cell surface as well as wild type GluR1. Functional and biochemical analyses indicated that these oligomerizing peptides specifically controlled the formation of the expected number of subunits in a channel complex. However, the channel function was only restored by the tetramer-forming peptide. Although the purified LIVBP domain of GluR1 formed a dimmer in solution, a dimer-forming peptide could not restore the function of GluR1. Moreover, a cross-linking assay indicated that four LIVBP domains are located in proximity to each other. These results suggest that the function of the LIVBP domain is not simply to form initial dimers but to adopt a conformation compatible with the overall tetrameric arrangement of subunits in intact AMPA receptors.

    DOI: 10.1074/jbc.M410513200

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  • PKC-independent inhibition of neuronal nicotinic acetylcholine receptors by diacylglycerol 査読

    T Andoh, H Itoh, T Higashi, Y Saito, D Ishiwa, Y Kamiya, Y Yamada

    BRAIN RESEARCH   1013 ( 1 )   125 - 133   2004年7月

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    記述言語:英語   掲載種別:研究論文(学術雑誌)   出版者・発行元:ELSEVIER SCIENCE BV  

    Diacylglycerol modulates cell functions primarily through activation of protein kinase C (PKC). In a previous study, however, we found that a diacylglycerol analogue. 1-oleoyl-2-acetylglycerol (OAG), accelerated desensitization of neuronal nicotinic acetylcholine receptors (nAchRs) independently of PKC activation in PC12 cells. In the present study, we investigated whether other analogues and endogenous diacylglycerol exert similar effects on neuronal nAchRs and characterized the modulation by diacylglycerol. We measured the nicotine-induced whole-cell current in the absence and presence of diacylglycerol analogues in PC12 cells. We also investigated the effects of a blockade of metabolic pathways of diacylglycerol by inhibiting diacylglycerol lipase and kinase. We found that all four diacylglycerol analogues studied promoted desensitization and depressed the nondesensitized component of the nicotine-induced Current. These effects seemed independent of PKC activation because they were not antagonized by the PKC inhibitors staurosporine or bisindolylmaleimide I; one analogue that lacks the PKC-stimulating action was also effective. The effects of diacylglycerol analogues were not antagonized by high doses of nicotine and were independent of the membrane potential. Similar modulatory effects were observed by treatment with RHC80267, a blocker of diacylglycerol lipase, and R59949, an inhibitor of diacylglycerol kinase, in the presence of staurosporme. These results Suggest that diacylglycerol, both exogenously applied and endogenously produced, modulates neuronal nAchRs independently of PKC activation in PC12 cells; further, these effects seemed consistent with a noncompetitive and voltage-independent block. They raised the possibility that PKC-independent inhibition of neuronal nAchRs by diacylglycerol may be a novel modulatory process. (C) 2004 Elsevier B.V. All rights reserved.

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  • Effects of isoflurane and ketamine on ATP-sensitive K channels in rat substantia nigra 査読

    D Ishiwa, Y Kamiya, H Itoh, Y Saito, T Ohtsuka, Y Yamada, T Andoh

    NEUROPHARMACOLOGY   46 ( 8 )   1201 - 1212   2004年6月

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    記述言語:英語   掲載種別:研究論文(学術雑誌)   出版者・発行元:PERGAMON-ELSEVIER SCIENCE LTD  

    Whole cell recordings were made using midbrain slices to examine the effects of, two different anaesthetics on ATP-sensitive K (K-ATP) channels in principle tiel,neurons Of rat substantia nigra pars compacta. When neurons were dialyzed with an ATP-free pipette solution during perfusion with a glucose-free external solution, a hyperpolarization and an outward current developed slowly in a tolbutamide-inhibitable manner. The volatile anaesthetic 3% isoflurane slightly depolarised the neurons in the presence of ATP in the pipette solution and glucose in the external solution. but it did not affect the hyperpolarization or outward current in response to omission of ATP and glucose. Ketamine, an intravenous anaesthetic, did not change the membrane potential when ATP and glucose were included however. it reversibly inhibited the hyperpolarization and outward current induced by intracellular ATP depletion in a dose-dependent manner. These effects of ketamine were not mimicked by AP-5, an NMDA receptor antagonist, or indatraline, an inhibitor of catecholamine uptake. These findings suggest that these anaesthetics have no stimulatory action on K-ATP channels in these neurons when intracellular ATP is preserved and that ketamine but not isoflurane inhibits K-ATP channels when the channels were activated by low intracellular ATP. (C) 2004 Elsevier Ltd. All rights reserved.

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  • Specific assembly with the NMDA receptor 3B subunit controls surface expression and calcium permeability of NMDA receptors 査読

    K Matsuda, M Fletcher, Y Kamiya, M Yuzaki

    JOURNAL OF NEUROSCIENCE   23 ( 31 )   10064 - 10073   2003年11月

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    記述言語:英語   掲載種別:研究論文(学術雑誌)   出版者・発行元:SOC NEUROSCIENCE  

    The NMDA receptor 3B (NR3B) subunit is the most recently identified member of the NMDA receptor family. In heterologous cells, it has been shown to reduce the Ca2+ permeability of glutamatergic receptor complexes formed together with NR1 and NR2 subunits and to form the unique excitatory glycine receptor complex with the NR1 subunit. However, it is unclear whether NR3B protein is expressed in and exerts similar functions in neurons. In addition, it is not understood how NR3B interacts with NR1 and NR2 and how such an interaction may regulate the membrane trafficking of the NMDA receptor complex. Here we report that our analysis using an antibody specific for NR3B showed that the NR3B protein is selectively expressed in somatic motor neurons in the brainstem of adult mice. Coimmunoprecipitation and electrophysiological analyses demonstrated that NR3B, when exogenously introduced into hippocampal neurons, can coassemble with endogenous NR1 and NR2A and can reduce the Ca2+ permeability of NMDA currents. In contrast, NR3B was not involved in the excitatory glycine response in neurons under our test conditions. Although NR1 or NR3B alone cannot be transported to the cell surface, coexpression of these subunits mutually supported transport of the NMDA receptor complex by interaction involving the specific regions of the C terminus of NR3B. These results indicate that NR3B may modulate the function of NMDA receptors in somatic motor neurons during adulthood by controlling membrane trafficking and by reducing Ca2+ permeability.

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  • Heteromer formation of δ2 glutamate receptors with AMPA or kainate receptors 査読

    Kazuhisa Kohda, Yoshinori Kamiya, Shinji Matsuda, Kunio Kato, Hisashi Umemori, Michisuke Yuzaki

    Molecular Brain Research   110 ( 1 )   27 - 37   2003年1月

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    記述言語:英語   掲載種別:研究論文(学術雑誌)   出版者・発行元:Elsevier {BV}  

    DOI: 10.1016/S0169-328X(02)00561-2

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  • Heteromer formation of delta 2 glutamate receptors with AMPA or kainate receptors 査読

    K Kohda, Y Kamiya, S Matsuda, K Kato, H Umemori, M Yuzaki

    MOLECULAR BRAIN RESEARCH   110 ( 1 )   27 - 37   2003年1月

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    記述言語:英語   掲載種別:研究論文(学術雑誌)   出版者・発行元:ELSEVIER SCIENCE BV  

    The 82 glutamate receptor (GluRdelta2) is predominantly expressed in the postsynaptic densities of parallel fiber-Purkinje cell synapses and plays a crucial role in cerebellar function. However, the mechanisms by which GluRdelta2 participates in cerebellar functions are largely unknown because GluRdelta2 does not bind glutamate analogs. We investigated the possibility that GluRdelta2 may be involved in channel formation together with other glutamate receptor families. We transiently expressed lurcher mutant AMPA receptor GluR1(Lc) and kainate receptor GluR6(Lc) in HEK293 cells. Cells expressing these constitutively active channels displayed a rectifying current-voltage (I-V) relationship. However, when cells were co-transfected with GluRdelta2(Lc), which had the arginine residue in the channel pore region, cells displayed a linear I-V relationship, a result that indicates GluRdelta2(Lc) formed functional heteromeric channels with GluR1(Lc) or GluR6(Lc). Assembly of GluRdelta2 with GluR1 or GluR6 was further confirmed by co-immunoprecipitation assays in HEK293 cells. In addition, GluRdelta2 receptors were partially co-immunoprecipitated from cerebellar synaptosomal fractions by antibodies against GluR2 or KA2. In contrast to lurcher channels. expression of wild-type GluRdelta2 significantly reduced the glutamate-induced current of the wild-type GluR1 receptors without affecting channel properties, such as current kinetics, dose-response relationship, and single-channel conductance. Thus, the heteromeric channel created by the association of wild-type GluR1 and GluRdelta2 may not be gated by glutamate and does not participate in glutamate-induced currents. These results suggest that GluRdelta2 and AMPA or kainate receptors can assemble to form heteromeric receptors in vitro and could modify glutamate signaling in vivo. These findings may help explain the role of GluRdelta2. (C) 2002 Elsevier Science B.V. All rights reserved.

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  • Inbibitory effects of isoflurane and nonimmobilizing halogenated compounds on neuronal nicotinic acetylcboline receptors 査読

    T Matsuura, Y Kamiya, H Itoh, T Higashi, Y Yamada, T Andoh

    ANESTHESIOLOGY   97 ( 6 )   1541 - 1549   2002年12月

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    記述言語:英語   掲載種別:研究論文(学術雑誌)   出版者・発行元:LIPPINCOTT WILLIAMS & WILKINS  

    Background: Neuronal nicotinic acetylcholine receptors (nAchRs) are inhibited by low concentrations of volatile anesthetics. However, it is not clear whether this phenomenon contributes to the anesthetic effects of volatile anesthetics. Effects of a volatile anesthetic (isoflurane) and structurally related nonimmobilizers (F6: 1,2-dichlorohexafluorocyclobutane, F8: 2,3-dichlorooctafluorobutane) on the current mediated through neuronal nAchRs were studied.
    Method This study investigated neuronal nAchRs in PC12 cells and acutely dissociated rat medial habenula (MHb) neurons. Whole cell currents elicited by 30 mum nicotine were recorded in the absence and presence of the halogenated agents. The minimum alveolar concentrations (MACS) for F6 and F8 were predicted from Meyer-Overton correlation.
    Results: All halogenated compounds inhibited the nicotine-induced current in a concentration-dependent manner in PC12 cells. In MHb neurons, while isoflurane and F6 significantly inhibited the nicotine-induced peak current, F8 failed to inhibit it. The peak currents in the presence of isoflurane at 1.7 MAC, of F6 at 2.4 MAC, and of F8 at 2.2 MAC were 12, 31, and 97% of control, respectively.
    Conclusions: Isoflurane, F6, and F8 inhibited ganglion-type nAchRs in PC12 cells independent from their abilities to produce the anesthetic state. In MHb neurons, isoflurane and F6, which lack the immobilizing effect but has the amnesic effect, inhibited nAchRs. Native brain nicotinic receptors in MHb neurons were almost insensitive to F8, which lacks both the immobilizing and the amnesic effect. These results are consistent with the hypothesis that inhibition of nAchRs in MHb neurons is not important for the anesthetic effect but may contribute to the amnesic effect of these agents.

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  • Cloning and characterization of a novel NMDA receptor subunit NR3B: a dominant subunit that reduces calcium permeability 査読

    K Matsuda, Y Kamiya, S Matsuda, M Yuzaki

    MOLECULAR BRAIN RESEARCH   100 ( 1-2 )   43 - 52   2002年4月

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    記述言語:英語   掲載種別:研究論文(学術雑誌)   出版者・発行元:ELSEVIER SCIENCE BV  

    We report the cloning and characterization of a novel NMDA receptor subunit cDNA, which encodes a predicted polypeptide of 1003 amino acids. Phylogenic analysis indicates that this new subunit is most closely related to NR3A. Therefore, we term it NR3B. Important functional domains of glutamate receptor,.;, such as the ligand-binding domain, the channel pore, and the channel gate, are conserved in NR3B. NR3B mRNA was expressed highly in pons, midbrain, medulla, and the spinal cord, but at low levels in the forebrain and the cerebellum. Although NR3A mRNA expression decreases sharply after the second postnatal weeks, NR3B mRNA expression levels in whole brain were constant during postnatal development and into adult. Coimmunoprecipitation analysis showed that NR3B could form NMDA receptor complex with NR1a and NR2A subunits in heterologous cells. Although expression of NR3B alone did not reconstitute functional NMDA receptors, coexpression of NR3B reduced the Ca2+ permeability of glutamate-induced currents in cells expressing NR1a and NR2A. These results indicate that NR3B is a dominant modulatory subunit that can modify the function of NMDA receptors. Since hi,h Ca2+ permeability of NMDA receptors is thought to be a key feature for NMDA receptors to play critical roles in neurodevelopment, synaptic plasticity, and neuronal death, NR3B may contribute to the regulation of these physiological and pathological processes. (C) 2002 Elsevier Science B.V. All rights reserved.

    DOI: 10.1016/S0169-328X(02)00173-0

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  • Cloning and characterization of a novel NMDA receptor subunit NR3B: a dominant subunit that reduces calcium permeability

    K Matsuda, Y Kamiya, S Matsuda, M Yuzaki

    MOLECULAR BRAIN RESEARCH   100 ( 1-2 )   43 - 52   2002年4月

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    記述言語:英語   掲載種別:研究論文(学術雑誌)   出版者・発行元:ELSEVIER SCIENCE BV  

    We report the cloning and characterization of a novel NMDA receptor subunit cDNA, which encodes a predicted polypeptide of 1003 amino acids. Phylogenic analysis indicates that this new subunit is most closely related to NR3A. Therefore, we term it NR3B. Important functional domains of glutamate receptor,.;, such as the ligand-binding domain, the channel pore, and the channel gate, are conserved in NR3B. NR3B mRNA was expressed highly in pons, midbrain, medulla, and the spinal cord, but at low levels in the forebrain and the cerebellum. Although NR3A mRNA expression decreases sharply after the second postnatal weeks, NR3B mRNA expression levels in whole brain were constant during postnatal development and into adult. Coimmunoprecipitation analysis showed that NR3B could form NMDA receptor complex with NR1a and NR2A subunits in heterologous cells. Although expression of NR3B alone did not reconstitute functional NMDA receptors, coexpression of NR3B reduced the Ca2+ permeability of glutamate-induced currents in cells expressing NR1a and NR2A. These results indicate that NR3B is a dominant modulatory subunit that can modify the function of NMDA receptors. Since hi,h Ca2+ permeability of NMDA receptors is thought to be a key feature for NMDA receptors to play critical roles in neurodevelopment, synaptic plasticity, and neuronal death, NR3B may contribute to the regulation of these physiological and pathological processes. (C) 2002 Elsevier Science B.V. All rights reserved.

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  • Inhibitory effects of barbiturates on nicotinic acetylcholine receptors in rat central nervous system neurons 査読

    Y Kamiya, T Andoh, Watanabe, I, T Higashi, H Itoh

    ANESTHESIOLOGY   94 ( 4 )   694 - 704   2001年4月

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    記述言語:英語   掲載種別:研究論文(学術雑誌)   出版者・発行元:LIPPINCOTT WILLIAMS & WILKINS  

    Background: Neuronal nicotinic acetylcholine receptors (nAChRs) are widely expressed in the central and autonomic nervous systems. The authors have previously shown that depressant and convulsant barbiturates both inhibit the ganglion-type nAchRs in PC12 cells. However, the central and ganglion-type receptors have different subunit composition and pharmacologic properties. In this study, the authors investigated the effects of thiopental, depressant [R(-)] and convulsant [S(+)] stereoisomers of 1-methyl-5 phenyl-5-propyl barbituric acid (MPPB) on neuronal nAChRs in the rat central nervous system to explore significance of these effects in barbiturate anesthesia.
    Methods: Whole-cell currents were measured in acutely dissociated rat medial habenula (MHb) neurons by applying 10 or 100 muM nicotine in the absence or presence of thiopental 3-100 muM. Effects of R(-)- and S(+)-MPPB on the nicotine-induced current were also studied.
    Results: Thiopental suppressed the nicotine-elicited inward current and accelerated the current decay dose-dependently at the clinical relevant concentrations. R(-)- and S(+)-MPPB both inhibited the nicotine-induced current dose-dependently without augmenting the current decay. There was no significant difference in the magnitudes of inhibition by R(-)- and S(+)-MPPB.
    Conclusions Although thiopental suppressed the current mediated through native nAchRs in rat MHb neurons at the clinically relevant concentrations, the depressant and convulsant stereoisomers of MPPB both inhibited the current in the same extent. These findings are consistent with the results previously obtained in the ganglion-type receptors of PC12 cells and suggest that inhibition of nAChRs in MHb neurons is not directly relevant to the hypnotic or anticonvulsive actions of barbiturates.

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  • Nonstereoselective inhibition of neuronal nicotinic acetylcholine receptors by ketamine isomers 査読

    T Sasaki, T Andoh, Watanabe, I, Y Kamiya, H Itoh, T Higashi, T Matsuura

    ANESTHESIA AND ANALGESIA   91 ( 3 )   741 - 748   2000年9月

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    記述言語:英語   掲載種別:研究論文(学術雑誌)   出版者・発行元:LIPPINCOTT WILLIAMS & WILKINS  

    We have found that racemic ketamine strongly inhibits the current mediated through neuronal nicotinic acetylcholine receptors (nAchRs) in PC12 cells, a rat pheochromocytoma cell line. Ketamine stereoisomers have different potencies for the anesthetic action, with the S-enantiomer being about 3 times as potent as the R-enantiomer. The purpose of this study was to clarify if the inhibitory effects of ketamine on neuronal nAchRs contribute to their anesthetic effect. We compared potencies of ketamine enantiomers for neuronal nAchR inhibition with those for the anesthetic action. S(+) and R(-) ketamine inhibited the nicotine-induced whole-cell current in a dose-dependent manner at the membrane potential of -60 mV. They accelerated the current decay, resulting in the larger effects on the nondesensitized current than on the peak current. There was no significant difference in the concentrations for 50% inhibition between the stereoisomers. The ketamine isomers exerted the same effects on single-channel properties estimated from analysis of the nicotine-induced current noise. These results indicate that the inhibitory action of ketamine isomers on neuronal nAchRs is not stereoselective. Although our findings do not deny possible involvement of these receptors in ketamine anesthesia, they suggest that inhibition of neuronal nAchRs is not primarily responsible for the anesthetic action of this anesthetic.

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  • Nonstereoselective inhibition of neuronal nicotinic acetylcholine receptors by ketamine isomers 査読

    T Sasaki, T Andoh, Watanabe, I, Y Kamiya, H Itoh, T Higashi, T Matsuura

    ANESTHESIA AND ANALGESIA   91 ( 3 )   741 - 748   2000年9月

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    記述言語:英語   掲載種別:研究論文(学術雑誌)   出版者・発行元:LIPPINCOTT WILLIAMS & WILKINS  

    We have found that racemic ketamine strongly inhibits the current mediated through neuronal nicotinic acetylcholine receptors (nAchRs) in PC12 cells, a rat pheochromocytoma cell line. Ketamine stereoisomers have different potencies for the anesthetic action, with the S-enantiomer being about 3 times as potent as the R-enantiomer. The purpose of this study was to clarify if the inhibitory effects of ketamine on neuronal nAchRs contribute to their anesthetic effect. We compared potencies of ketamine enantiomers for neuronal nAchR inhibition with those for the anesthetic action. S(+) and R(-) ketamine inhibited the nicotine-induced whole-cell current in a dose-dependent manner at the membrane potential of -60 mV. They accelerated the current decay, resulting in the larger effects on the nondesensitized current than on the peak current. There was no significant difference in the concentrations for 50% inhibition between the stereoisomers. The ketamine isomers exerted the same effects on single-channel properties estimated from analysis of the nicotine-induced current noise. These results indicate that the inhibitory action of ketamine isomers on neuronal nAchRs is not stereoselective. Although our findings do not deny possible involvement of these receptors in ketamine anesthesia, they suggest that inhibition of neuronal nAchRs is not primarily responsible for the anesthetic action of this anesthetic.

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  • Dynorphins directly inhibit neuronal nicotinic acetylcholine receptors in PC12 calls 査読

    H Itoh, T Andoh, Watanabe, I, T Sasaki, Y Kamiya, F Okumura

    EUROPEAN JOURNAL OF NEUROSCIENCE   12 ( 4 )   1253 - 1262   2000年4月

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    記述言語:英語   掲載種別:研究論文(学術雑誌)   出版者・発行元:BLACKWELL SCIENCE LTD  

    The authors have previously reported that dynorphin A (1-17), an endogenous kappa opioid agonist, inhibits the current mediated through neuronal nicotinic acetylcholine receptors (nAChRs) without the involvement of opioid receptors or G-proteins. We have further characterized this action to elucidate the mechanisms. The nicotine-induced current was studied in PC12 cells using patch-clamp techniques. In the whole-cell configuration, four kinds of dynorphins with different lengths, dynorphin A (1-17) (1-13) (2-13) and (1-8), similarly inhibited the nicotine-induced inward current at 1 mu M and accelerated the current decay. The inhibition by dynorphin A (1-17) was not antagonized by the increasing concentrations of nicotine. The current-voltage relationship revealed that dynorphin's inhibition was voltage independent at the membrane potentials from -30 to -70 mV. The inhibition was not affected by pretreatment with pertussis toxin (PTX) or inclusion of staurosporine into the pipette solution. The inhibitory effect of dynorphin A (1-17) was well preserved in the outside-out patch configuration. Analysis of the nicotine-induced noise and single-channel kinetics revealed that dynorphin A (1-17) reduced open time without changing the amplitude of the unitary current. We found that the inhibitory effect on neuronal nAChRs is shared by all four dynorphins studied. The inhibition appears to be non-competitive and voltage independent. The outside-out recording together with other experiments indicated that a major part of this inhibition is not mediated through cytoplasmic messengers, but based on the direct action of dynorphins on neuronal nAChRs leading to the reduction of open time.

    DOI: 10.1046/j.1460-9568.2000.00012.x

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  • Comparison of the effects of convulsant and depressant barbiturate stereoisomers on AMPA-type glutamate receptors 査読

    Y Kamiya, T Andoh, R Furuya, S Hattori, Watanabe, I, T Sasaki, H Ito, F Okumura

    ANESTHESIOLOGY   90 ( 6 )   1704 - 1713   1999年6月

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    記述言語:英語   掲載種別:研究論文(学術雑誌)   出版者・発行元:LIPPINCOTT WILLIAMS & WILKINS  

    Background: alpha-Amino-3-hydroxy-5-methyl-4-isoxazole propionic acid (AMPA)-type glutamate receptors mediate fast excitatory synaptic transmission in the central nervous system. Although barbiturates have been shown to suppress the AMPA receptor-mediated responses, it is unclear whether this effect contributes to the anesthetic action of barbiturates. The authors compared the effects of depressant [R(-)] and convulsant [S(+)] stereoisomers of 1-methyl-5-phenyl-5-propyl barbituric acid (MPPB) on the AMPA and gamma-aminobutyric acid type A (GABA(A)) receptor-mediated currents to determine if the inhibitory effects on AMPA receptors correlate to the in vivo effects of the isomers.
    Method: The authors measured whole-cell currents in the rat cultured cortical neuron at holding potential of -60 mV. Kainate 500 mu M mas applied as the agonist for AMPA receptors. Thiopental (3-300 mu M), R(-)-MPPB or S(+)-MPPB (100-1,000 mu M) was coapplied with kainate under the condition in which the GABA, receptor-mediated current was blocked. Effects of MPPB isomers on the current elicited by GABA 1 mu M were studied in the separate experiments.
    Results: Thiopental inhibited the kainate-induced current reversibly and in a dose-dependent manner, with a concentration for 50% inhibition of 49.3 mu M. Both R(-)-MPPB and S(S)-MPPB inhibited the kainate-induced current with a little stereoselectivity. R(-)-MPPB was slightly but significantly more potent than S(+)-MPPB. In contrast, R(-)-,MPPB enhanced but S(+)-MPPB reduced the GABA-induced current.
    Conclusions: Both convulsant and depressant stereoisomers of the barbiturate inhibited the AMPA receptor-mediated current despite of their opposite effects oil the central nervous system in vivo. Although thiopental exhibited a considerable inhibition of AMPA receptors, the results suggest that the inhibition of AMPA receptors contributes little to the hypnotic action of the barbiturates.

    DOI: 10.1097/00000542-199906000-00028

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  • Depressant and convulsant barbiturates both inhibit neuronal nicotinic acetylcholine receptors 査読

    Watanabe, I, T Andoh, R Furuya, T Sasaki, Y Kamiya, H Itoh

    ANESTHESIA AND ANALGESIA   88 ( 6 )   1406 - 1411   1999年6月

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    記述言語:英語   掲載種別:研究論文(学術雑誌)   出版者・発行元:LIPPINCOTT WILLIAMS & WILKINS  

    Neuronal nicotinic acetylcholine receptors (neuronal nAchRs) are sensitive to many anesthetics, including barbiturates, which suggests that these receptors are potential sites for anesthetic action. Subtle changes in molecular structures of the anesthetic barbiturates can produce compounds with potent convulsant activity. Whereas R(-) isomer of 1-methyl-5-phenyl-5-propyl barbituric acid (MPPB) exerts anesthetic action, S(+)MPPB exhibits pure excitatory effects, including convulsion. 5-(2-cyclohexilidene-ethyl)-5-ethyl barbituric acid is another example of a convulsant barbiturate. We compared the effects of depressant and convulsant barbiturates on the neuronal nAchR-mediated current to determine whether inhibition of neuronal nAchRs contributes to the anesthetic action of barbiturates. Whole cell nicotine-induced currents were recorded in PC12 derived from rat pheochromocytoma, using the conventional whole cell patch clamp technique in the presence and absence of barbiturates. Both depressant and convulsant barbiturates inhibited the nicotine-induced inward current reversibly and in a dose-dependent manner when co-applied with nicotine. All barbiturates accelerated the current decay. There was no significant difference between the concentrations for 50% inhibition for MPPB isomers. There was no correlation between inhibition of ganglionic nAchRs and anesthetic effects of the barbiturates. These results strongly oppose the idea that inhibition of neuronal nAchRs contributes to the anesthetic action of barbiturates. Implications: We found that both convulsant and depressant barbiturates inhibit the current mediated through ganglionic nicotinic acetylcholine receptors in PC12 cells. This finding suggests that the inhibition of neuronal nicotinic acetylcholine receptors does not contribute to the anesthetic action of barbiturates.

    DOI: 10.1213/00000539-199906000-00038

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  • Depressant and convulsant barbiturates both inhibit neuronal nicotinic acetylcholine receptors 査読

    Watanabe, I, T Andoh, R Furuya, T Sasaki, Y Kamiya, H Itoh

    ANESTHESIA AND ANALGESIA   88 ( 6 )   1406 - 1411   1999年6月

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    記述言語:英語   掲載種別:研究論文(学術雑誌)   出版者・発行元:LIPPINCOTT WILLIAMS & WILKINS  

    Neuronal nicotinic acetylcholine receptors (neuronal nAchRs) are sensitive to many anesthetics, including barbiturates, which suggests that these receptors are potential sites for anesthetic action. Subtle changes in molecular structures of the anesthetic barbiturates can produce compounds with potent convulsant activity. Whereas R(-) isomer of 1-methyl-5-phenyl-5-propyl barbituric acid (MPPB) exerts anesthetic action, S(+)MPPB exhibits pure excitatory effects, including convulsion. 5-(2-cyclohexilidene-ethyl)-5-ethyl barbituric acid is another example of a convulsant barbiturate. We compared the effects of depressant and convulsant barbiturates on the neuronal nAchR-mediated current to determine whether inhibition of neuronal nAchRs contributes to the anesthetic action of barbiturates. Whole cell nicotine-induced currents were recorded in PC12 derived from rat pheochromocytoma, using the conventional whole cell patch clamp technique in the presence and absence of barbiturates. Both depressant and convulsant barbiturates inhibited the nicotine-induced inward current reversibly and in a dose-dependent manner when co-applied with nicotine. All barbiturates accelerated the current decay. There was no significant difference between the concentrations for 50% inhibition for MPPB isomers. There was no correlation between inhibition of ganglionic nAchRs and anesthetic effects of the barbiturates. These results strongly oppose the idea that inhibition of neuronal nAchRs contributes to the anesthetic action of barbiturates. Implications: We found that both convulsant and depressant barbiturates inhibit the current mediated through ganglionic nicotinic acetylcholine receptors in PC12 cells. This finding suggests that the inhibition of neuronal nicotinic acetylcholine receptors does not contribute to the anesthetic action of barbiturates.

    DOI: 10.1097/00000539-199906000-00038

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  • The effects of ketamine and propofol on neuronal nicotinic acetylcholine receptors and P-2X purinoceptors in PC12 cells 査読

    R Furuya, K Oka, Watanabe, I, Y Kamiya, H Itoh, T Andoh

    ANESTHESIA AND ANALGESIA   88 ( 1 )   174 - 180   1999年1月

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    記述言語:英語   掲載種別:研究論文(学術雑誌)   出版者・発行元:LIPPINCOTT WILLIAMS & WILKINS  

    We studied the effects of ketamine and propofol on two Ligand-gated ion channels mediating fast synaptic transmission through sympathetic ganglia, neuronal nicotinic acetylcholine receptors (nAchRs), and P-2x purinoceptors in a rat pheochromocytoma cell line PC12 using whole cell voltage clamp recording. Ketamine and propofol similarly inhibited the nicotine-induced inward current reversibly and dose-dependently at the membrane potential of -60 mV but had no effects on the adenosine triphosphate-induced current. Both anesthetics accelerated the current decay during agonist application, resulting in greater inhibition on the steady current than the peak current. The 50% inhibition concentration values for the steady current were lower than the clinically relevant concentrations for ketamine (2.8 +/- 0.6 mu M) and higher than those for propofol (5.4 +/- 0.6 mu M). Both anesthetics induced an addition of the fast component to the decay phase and an acceleration of the slow component, which suggests an open channel blockade or an enhancement of desensitization as a mechanism. The effects on closed channels seemed to be small because preincubation with the anesthetics did not significantly augment the block. Inhibition was voltage-independent at membrane potentials between -20 and -70 mV and was consistent with a noncompetitive block. Inhibition of the neuronal nAchR-mediated current may lead to the suppression of synaptic transmission in sympathetic ganglia by ketamine, but not by propofol, at the clinically relevant concentrations. However, these results are not consistent with changes in sympathetic nerve activities reported for animals or humans anesthetized with ketamine or propofol, which suggests effects from other systems, such as the central nervous system in vivo. Implications: Ketamine (at smaller than clinically relevant concentrations) and propofol (at larger than clinically relevant concentrations) inhibited neuronal nicotinic acetylcholine receptor-mediated current in PC12 cells, which possess the receptors that resemble those in post-ganglionic sympathetic neurons. These findings are not consistent with in vivo experiments, which suggests that effects from other systems, such as the central nervous system, are of importance.

    DOI: 10.1213/00000539-199901000-00033

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  • The effects of ketamine and propofol on neuronal nicotinic acetylcholine receptors and P-2X purinoceptors in PC12 cells 査読

    R Furuya, K Oka, Watanabe, I, Y Kamiya, H Itoh, T Andoh

    ANESTHESIA AND ANALGESIA   88 ( 1 )   174 - 180   1999年1月

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    記述言語:英語   掲載種別:研究論文(学術雑誌)   出版者・発行元:LIPPINCOTT WILLIAMS & WILKINS  

    We studied the effects of ketamine and propofol on two Ligand-gated ion channels mediating fast synaptic transmission through sympathetic ganglia, neuronal nicotinic acetylcholine receptors (nAchRs), and P-2x purinoceptors in a rat pheochromocytoma cell line PC12 using whole cell voltage clamp recording. Ketamine and propofol similarly inhibited the nicotine-induced inward current reversibly and dose-dependently at the membrane potential of -60 mV but had no effects on the adenosine triphosphate-induced current. Both anesthetics accelerated the current decay during agonist application, resulting in greater inhibition on the steady current than the peak current. The 50% inhibition concentration values for the steady current were lower than the clinically relevant concentrations for ketamine (2.8 +/- 0.6 mu M) and higher than those for propofol (5.4 +/- 0.6 mu M). Both anesthetics induced an addition of the fast component to the decay phase and an acceleration of the slow component, which suggests an open channel blockade or an enhancement of desensitization as a mechanism. The effects on closed channels seemed to be small because preincubation with the anesthetics did not significantly augment the block. Inhibition was voltage-independent at membrane potentials between -20 and -70 mV and was consistent with a noncompetitive block. Inhibition of the neuronal nAchR-mediated current may lead to the suppression of synaptic transmission in sympathetic ganglia by ketamine, but not by propofol, at the clinically relevant concentrations. However, these results are not consistent with changes in sympathetic nerve activities reported for animals or humans anesthetized with ketamine or propofol, which suggests effects from other systems, such as the central nervous system in vivo. Implications: Ketamine (at smaller than clinically relevant concentrations) and propofol (at larger than clinically relevant concentrations) inhibited neuronal nicotinic acetylcholine receptor-mediated current in PC12 cells, which possess the receptors that resemble those in post-ganglionic sympathetic neurons. These findings are not consistent with in vivo experiments, which suggests that effects from other systems, such as the central nervous system, are of importance.

    DOI: 10.1097/00000539-199901000-00033

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  • Inhibition of the neuronal nicotinic receptor-mediated current by kappa opioid receptor agonists in PC12 cells 査読

    Keikou Oka, Tomio Andoh, Itaru Watanabe, Yoshinori Kamiya, Hideki Ito

    Pflugers Archiv European Journal of Physiology   436 ( 6 )   887 - 893   1998年

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    記述言語:英語   掲載種別:研究論文(学術雑誌)   出版者・発行元:Springer Science $\mathplus$ Business Media  

    The authors studied effects of opioid receptor agonists on neuronal nicotinic-receptor-mediated current in PC12 cells using whole-cell current recording. At 1 μM, [D-Ala, N-Me, Phe, Gly-ol]- enkephalin (DAMGO), a selective μ receptor agonist, or 10 μM methionine-enkephalin, a μ and δ receptor agonist, did not inhibit the current elicited by 30 μM nicotine significantly. Dynorphin A (1-17) (0.1-1 μM), an endogenous κ receptor agonist, and U50488 (0.1-10 μM), a non-peptide selective κ receptor agonist, depressed the nicotine-induced current reversibly in a dose- dependent manner. They accelerated the current decay, resulting in greater effects on the nondesensitized current than the peak current. These effects were not affected by nor-binaltrophimine, a selective κ receptor antagonist, or by inclusion of guanosine 5'-O-(2-thiobiphosphate) (GDP[β-S]), a GTP binding protein blocker, into the pipette solution. These results demonstrate that two κ opioid receptor agonists, dynorphin A (1-17) and U50488, inhibit neuronal nicotinic-receptor-mediated current without the involvement of opioid receptors or GTP binding proteins. The acceleration of the current decay suggests a direct action on nicotinic receptors such as open channel block, or augmentation of desensitization. Modulation of neuronal nicotinic receptors by dynorphins may play a role in some areas where dynorphin release sites and neuronal nicotinic receptors are colocalized.

    DOI: 10.1007/s004240050719

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  • Differential effects of thiopental on neuronal nicotinic acetylcholine receptors and P-2X purinergic receptors in PC12 cells 査読

    T Andoh, R Furuya, K Oka, S Hattori, Watanabe, I, Y Kamiya, F Okumura

    ANESTHESIOLOGY   87 ( 5 )   1199 - 1209   1997年11月

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    記述言語:英語   掲載種別:研究論文(学術雑誌)   出版者・発行元:LIPPINCOTT-RAVEN PUBL  

    Background: PC12 cells, derived from rat pheochromocytoma, express neuronal nicotinic acetylcholine receptors (nAchRs) and P-2x, purinergic receptors, both of which resemble the receptors in postganglionic sympathetic neurons. The former is the established and the latter is the putative receptor to mediate fast synaptic transmission. The authors investigated effects of thiopental on these two ligand-gated ion channels.
    Methods: Whole cell currents were recorded in PC12 cells without treatment of nerve growth factor, using conventional whole cell patch clamp technique. Nicotine or adenosine triphosphate (ATP) 30 mu M was applied for 4-5 s in the absence or presence of thiopental 3-300 mu M.
    Results: Nicotine induced the rapidly decaying inward current at -60 mV, which exhibited the characteristics of the neuronal nAchR-mediated current. Thiopental inhibited the nicotine-induced inward current and accelerated the current decay in a dose-dependent manner, resulting in the greater effects on the steady current than the peak current. IC50s for the peak and steady current were 56.7 and 7.4 mu M, when the anesthetic was coapplied with nicotine. Thiopental's inhibition was not associated with a change in the reversal potential and was voltage-independent at membrane potential of -30 to -70 mV. Most of thiopental's effects seemed to require channel opening. In contrast to the nicotine-induced current, thiopental had little effect on the current elicited by ATP.
    Conclusions: Thiopental, whose reported EC50 for general anesthesia is 25 mu M, inhibited the neuronal nAchR-mediated current but not the P-2x receptor-mediated response in PC12 cells at clinically relevant concentrations. Inhibition may result in suppression of synaptic transmission in sympathetic ganglia.

    DOI: 10.1097/00000542-199711000-00025

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  • アミロイドベータはCollapsin Response Mediator Protein 2のリン酸化を介して神経毒性を発現する

    磯野 俊成, 山下 直也, 紙谷 義孝, Alkam Tursun, 新田 淳美, 鍋島 俊隆, 五嶋 良郎

    日本薬理学雑誌   142 ( 4 )   1P - 1P   2013年10月

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    記述言語:日本語   出版者・発行元:(公社)日本薬理学会  

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  • A reply

    Y. Koyama, M. Nishihama, G. Inagawa, Y. Kamiya, T. Miki, R. Kurihara, T. Goto

    Anaesthesia   67 ( 4 )   435 - 436   2012年4月

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    記述言語:英語   掲載種別:速報,短報,研究ノート等(学術雑誌)  

    DOI: 10.1111/j.1365-2044.2012.07071_2.x

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  • Hippocampus-dependent learning requires synaptic AMPA receptor delivery: effect of delivery blocking in behaving rats

    Dai Mitsushima, Kouji Ishihara, Yoshinori Kamiya, Takuya Takahashi

    JOURNAL OF PHYSIOLOGICAL SCIENCES   60   S84 - S84   2010年

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    記述言語:英語   掲載種別:研究発表ペーパー・要旨(国際会議)   出版者・発行元:SPRINGER TOKYO  

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  • Learning requires synaptic delivery of AMPA receptors at CA3-CA1 synapses

    Dai Mitsushima, Kouji Ishihara, Yoshinori Kamiya, Takuya Takahashi

    NEUROSCIENCE RESEARCH   65   S68 - S68   2009年

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    記述言語:英語   掲載種別:研究発表ペーパー・要旨(国際会議)   出版者・発行元:ELSEVIER IRELAND LTD  

    DOI: 10.1016/j.neures.2009.09.219

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  • LEARNING REQUIRES SYNAPTIC DELIVERY OF AMPA RECEPTORS AT SCHAFFER COLLATERAL SYNAPSES IN THE DORSAL HIPPOCAMPUS

    Dai Mitsushima, Kouji Ishihara, Yoshinori Kamiya, Takuya Takahashi

    JOURNAL OF PHYSIOLOGICAL SCIENCES   59   176 - 176   2009年

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    記述言語:英語   掲載種別:研究発表ペーパー・要旨(国際会議)   出版者・発行元:SPRINGER TOKYO  

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  • L-DOPA affects field excitatory postsynaptic potentials in rats NTS

    Momo Fujii, Yasuhiro Murota, Yoshinori Kamiya, Yoshio Goshima

    JOURNAL OF PHARMACOLOGICAL SCIENCES   109   130P - 130P   2009年

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    記述言語:英語   掲載種別:研究発表ペーパー・要旨(国際会議)   出版者・発行元:JAPANESE PHARMACOLOGICAL SOC  

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  • Acetylcholine release during learning mediates synaptic delivery of AMPA receptors into Schaffer collateral synapses in the dorsal hippocampus

    Dai Mitsushima, Kouji Ishihara, Yoshinori Kamiya, Takuya Takahashi

    NEUROSCIENCE RESEARCH   61   S68 - S68   2008年

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    記述言語:英語   掲載種別:研究発表ペーパー・要旨(国際会議)   出版者・発行元:ELSEVIER IRELAND LTD  

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  • パーキンソン病モデルラット脳内における移植皮膚由来幹細胞のドーパミンニューロンへの分化

    東田 哲博, 久保 篤彦, 菅野 洋, 美津島 大, 實木 亨, 紙谷 義孝, 山本 勇夫

    日本脳神経外科学会総会CD-ROM抄録集   66回   3I - O42   2007年10月

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    記述言語:日本語   出版者・発行元:(一社)日本脳神経外科学会  

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  • Effects of convulsant and depressant barbiturate stereoisomers on neuronal nicotinic acetylcholine receptors in rat CNS neurons

    Y Kamiya, T Andoh, Watanabe, I, T Higashi, F Okumura

    ANESTHESIOLOGY   93 ( 3A )   U190 - U190   2000年9月

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    記述言語:英語   掲載種別:研究発表ペーパー・要旨(国際会議)   出版者・発行元:LIPPINCOTT WILLIAMS & WILKINS  

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  • Inhibitory effects of isoflurane and nonimmobilizing halogenated compounds on neuronal nicotinic receptors

    T Matsuura, T Andoh, Y Kamiya, H Itoh, F Okumura

    ANESTHESIOLOGY   93 ( 3A )   U190 - U190   2000年9月

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    記述言語:英語   掲載種別:研究発表ペーパー・要旨(国際会議)   出版者・発行元:LIPPINCOTT WILLIAMS & WILKINS  

    Web of Science

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  • Effects of ketamine stereoisomers on neuronal nicotinic acetylcholine receptors

    T Andoh, T Sasaki, Wtanabe, I, Y Kamiya, F Okumura

    ANESTHESIOLOGY   91 ( 3A )   U361 - U361   1999年9月

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    記述言語:英語   掲載種別:研究発表ペーパー・要旨(国際会議)   出版者・発行元:LIPPINCOTT WILLIAMS & WILKINS  

    Web of Science

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  • Inhibitory effects of thiopental on neuronal nicotinic acetylcholine receptors in acutely dissociated rat CNS neurons

    Y Kamiya, Watanabe, I, T Andoh, F Okumura

    ANESTHESIOLOGY   91 ( 3A )   U362 - U362   1999年9月

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    記述言語:英語   掲載種別:研究発表ペーパー・要旨(国際会議)   出版者・発行元:LIPPINCOTT WILLIAMS & WILKINS  

    Web of Science

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  • Comparison of the effects of convulsant and depressant barbiturates on AMPA type glutamate receptors

    Y Kamiya, T Andoh, R Furuya, H Itou, F Okumura

    ANESTHESIOLOGY   89 ( 3A )   U758 - U758   1998年9月

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    記述言語:英語   掲載種別:研究発表ペーパー・要旨(国際会議)   出版者・発行元:LIPPINCOTT WILLIAMS & WILKINS  

    Web of Science

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  • Inhibitory effects of thiopental, ketamine, and propofol on neuronal nicotinic acetylcholine receptors in PC12 cells.

    R Furuya, T Andoh, K Oka, Y Kamiya, F Okumura

    ANESTHESIOLOGY   87 ( 3 )   A620 - A620   1997年9月

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    記述言語:英語   掲載種別:研究発表ペーパー・要旨(国際会議)   出版者・発行元:LIPPINCOTT-RAVEN PUBL  

    Web of Science

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  • Inhibition of neuronal nicotinic receptor-mediated current by kappa opioid receptor agonists

    T Andoh, K Oka, Y Kamiya, Watanabe, I, F Okumura

    ANESTHESIOLOGY   87 ( 3 )   A644 - A644   1997年9月

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    記述言語:英語   掲載種別:研究発表ペーパー・要旨(国際会議)   出版者・発行元:LIPPINCOTT-RAVEN PUBL  

    Web of Science

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▶ 全件表示

講演・口頭発表等

  • 反発性神経ガイダンス因子 Sema3A による神経因性疼痛軽減作用

    日本麻酔科学会第53回学術集会  2006年 

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    会議種別:ポスター発表  

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  • Intrathecally administered Sema3A protein attenuates neuropathic pain behavior in CCI model rats

    2006 Annual Meeting of American Society of Anesthesiologists  2006年 

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    会議種別:ポスター発表  

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共同研究・競争的資金等の研究

  • オピオイド鎮痛は遷延性術後痛の原因となるか?ー脊髄アストログリア活性化との関係ー

    研究課題/領域番号:20K09215  2020年4月 - 2023年3月

    日本学術振興会  科学研究費助成事業 基盤研究(C)  基盤研究(C)

    佐々木 美佳, 馬場 洋, 紙谷 義孝

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    配分額:4420000円 ( 直接経費:3400000円 、 間接経費:1020000円 )

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  • 特定神経ネットワークの人工的制御技術を駆使した全身麻酔薬の作用機序の解明

    研究課題/領域番号:19K22652  2019年6月 - 2021年3月

    日本学術振興会  科学研究費助成事業 挑戦的研究(萌芽)  挑戦的研究(萌芽)

    紙谷 義孝, 佐々木 美佳, 倉部 美起, 上野 将紀

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    配分額:6240000円 ( 直接経費:4800000円 、 間接経費:1440000円 )

    本研究の目的:全身麻酔時の意識消失や覚醒に深く関与しているとされている青斑核に注目し、覚醒下の動物において麻酔薬を投与した際の意識消失から覚醒までの一連の経過を解析することで、意識消失・覚醒のメカニズムにおける青斑核ニューロンの役割を解明することである。
    当該年度の研究内容:青斑核NA(ノルアドレナリン)ニューロンを特異的に制御可能なラットの作成を行った。NA神経特異的プロモーターを用いたアデノ随伴ウイルス(AAVPRSx8/hM3Dq)を作製し、このAAVを用いてhM3Dqがラット青斑核特異的に発現することを免疫組織学的に確認した。次に、AAV導入後のラットを用いて、青斑核NAニューロンをCNO腹腔内投与によって人為的に興奮させた際の、全身麻酔の作用を行動学的および電気生理学的に解析した。その結果、CNO投与によって揮発性麻酔薬による麻酔導入・覚醒時間はわずかに変化するのみであった。一方で、静脈麻酔薬(プロポフォール)による麻酔導入時間は著明に延長し、覚醒時間も著明に短縮した。電気生理学的解析には、当初予定していた覚醒状態での記録が困難であったことから、まずウレタン麻酔下で麻酔薬を投与した。その結果、青斑核ニューロンの活動電位に対する揮発性麻酔薬の影響には一定の傾向が認められなかったが、プロポフォール投与によって活動電位は著しく減少した。さらにCNO投与によって、プロポフォール投与時の活動電位は増加した。
    意義・重要性:揮発性麻酔薬と静脈麻酔薬(プロポフォール)とで、青斑核NAニューロンの応答様式は異なった。また、人為的な青斑核活性化は、プロポフォールの麻酔作用を劇的に変化させたが、揮発性麻酔薬の作用に明らかな変化を及ぼさなかった。
    プロポフォールは揮発性麻酔薬に比べて、より青斑核特異的な作用を持つ可能性が示唆された。

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  • 脱分化脂肪細胞由来の細胞抽出物による末梢神経損傷の新たな治療法開発

    研究課題/領域番号:19H03850  2019年4月 - 2023年3月

    日本学術振興会  科学研究費助成事業 基盤研究(B)  基盤研究(B)

    瀬尾 憲司, 田沼 順一, 前田 健康, 岸本 直隆, 武内 恒成, 紙谷 義孝, 山田 友里恵

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    配分額:17290000円 ( 直接経費:13300000円 、 間接経費:3990000円 )

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  • 神経障害性疼痛における脊髄・脳連関の生理学的解析およびグリア細胞活性化機構の解明

    2019年4月 - 2022年3月

    科学研究費補助金 

    紙谷 義孝

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    担当区分:研究代表者  資金種別:競争的資金

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  • ヘッジホッグシグナル伝達系は末梢神経再生を誘導する

    研究課題/領域番号:15H05041  2015年4月 - 2019年3月

    日本学術振興会  科学研究費補助金  基盤研究(B)

    瀬尾 憲司

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    資金種別:競争的資金

    末梢神経が損傷するとソニックヘッジホッグ(Shh)とその転写因子Gli1が神経損傷部に発現する。Shhシグナル系を抑制すると、再生軸索は異常に走行し、軸索結合は障害される。さらに中枢側断端の幼若シュワン細胞数を増加させ、末梢側でマクロファージ数を減少させる。損傷後の経過では、Shhの発現は損傷後早期に上昇し後期に減衰するが、Dhhは損傷後早期に発現量が低下し後期になると上昇する。Ihhは損傷前後では発現しない。すなわち損傷を契機にDhhシグナルからShhシグナルへのスイッチングが起こっている。
    以上の結果から損傷神経の再生にはShh,Dhhが重要な役割をしていることが示唆された。

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  • カルシウム感受性蛍光タンパクを用いたスライス及びin vivo脊髄イメージング

    研究課題/領域番号:15K15565  2015年4月 - 2017年3月

    日本学術振興会  科学研究費補助金  挑戦的萌芽研究

    紙谷 義孝

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    担当区分:研究代表者  資金種別:競争的資金

    本研究は脊髄後角における神経活動を二次元的に測定する目的で、アデノ随伴ウイルス(AAV)ベクターを用いて脊髄後角および後根神経節(DRG)にカルシウム感受性蛍光タンパク質を導入することを目的とした。髄腔内に接種したAAVベクターは、投与後1~2週間で、脊髄後角およびDRGにおいて標識タンパクであるTurboRFPを発現させる可能性があることを見出した。 しかし、免疫組織学的技術の限界のために、導入遺伝子由来タンパクが脊髄後角およびDRGにおいて確実に発現されたという確認は困難だった。 そのため、その先に計画した生理学的実験の結論は明らかにできなかった。

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  • μオピオイドによる急性耐性、痛覚過敏の細胞内シグナル機序の解明

    研究課題/領域番号:26293343  2014年4月 - 2018年3月

    日本学術振興会  科学研究費補助金  基盤研究(B)

    河野 達郎

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    資金種別:競争的資金

    オピオイド鎮痛薬は強力な鎮痛薬であるが、鎮痛効果の急速な減弱(急性耐性)や痛みの増強(痛覚過敏)を引き起こすことが報告されている。しかし、これらの現象は機序が明らかにされていないだけでなく、その存在さえも議論の分かれるところである。脊髄スライス標本およびin vivo脊髄標本へのレミフェンタニルの脊髄への灌流投与は興奮性シナプス後電流の頻度を減少させたが、投与終了後に頻度の増加は認められなかった。これらの結果から、レミフェンタニルは脊髄後角ニューロンのμオピオイド受容体を介して、興奮性シナプス伝達を抑制することがわかった。しかし、これまで言われている急性耐性や痛覚過敏は確認できなかった。

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  • 幼若脳に対する麻酔薬の興奮作用と神経毒性との関係の解明

    研究課題/領域番号:25462408  2013年4月 - 2017年3月

    日本学術振興会  科学研究費補助金  基盤研究(C)

    石和 大

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    資金種別:競争的資金

    多くの麻酔薬が幼若脳に広範なアポトーシスを生じることが報告されているが、その機序の全容は明らかではない。GABAA受容体は幼若脳では脱分極性の反応を生じ、GABAA受容体刺激作用のある麻酔薬は、興奮作用を示す可能性がある。私たちはCl-共輸送担体によるCl-排泄機構の変化およびそれに伴うGABA受容体の脱抑制が細胞毒性に関与しているのではないかと考えた。
    実験の結果、①未成熟期にミダゾラム投与を行い、成長期以降に社会的行動が阻害された、②組織学に脳機能への影響を包括的に評価した、③Cl-共輸送担体の一つであるKCC2の選択的活性化薬剤であるCLP290を投与することで、これらの現象が抑制された。

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  • 損傷を受けた神経細胞に対する麻酔・鎮静薬の毒性に関する検討

    2013年4月 - 2016年3月

    日本学術振興会  科学研究費補助金 

    安藤 富男

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    資金種別:競争的資金

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  • 成体ラット開腹手術モデルを用いた急性侵害性疼痛による記憶学習能への影響の検討

    研究課題/領域番号:25462409  2013年4月 - 2016年3月

    日本学術振興会  科学研究費補助金  基盤研究(C)

    小川 賢一

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    資金種別:競争的資金

    吸入麻酔薬を用いた全身麻酔手術後に生じる術後認知障害は,手術後の生存率と生活の質に悪影響を及ぼすことが知られている。本研究では下腹部開腹による術後疼痛モデルを作成し、遠隔期の文脈的記憶学習障害について検証を行ったところ、開腹術のみの侵襲では障害を生じない可能性が示唆された。また、5分間の吸入麻酔によって遠隔期に海馬AMPA受容体のシナプス発現量に変化を生じるが、開腹手術による侵害の影響は生じていない可能性が示唆された。これらは、臨床上の吸入麻酔薬の安全な使用法を開発していくうえで重要な知見であり、今後は遠隔期の認知記憶能の変化について、更なるデータの蓄積が必要と考えられる。

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  • 疼痛制御に関与するSema3Aシグナルパスウェイの解明

    2012年4月 - 2015年3月

    日本学術振興会  科学研究費補助金 

    紙谷 義孝

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    担当区分:研究代表者  資金種別:競争的資金

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  • 神経障害性疼痛モデル動物におけるシナプス可塑性の解析

    研究課題/領域番号:24791610  2012年4月 - 2014年3月

    日本学術振興会  科学研究費助成事業 若手研究(B)  若手研究(B)

    宮崎 智之, 紙谷 義孝

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    配分額:3900000円 ( 直接経費:3000000円 、 間接経費:900000円 )

    SNL術後早期に、脊髄後角第II層においてpCREBの一時的な低下が生じ、7日目以降正常化する。この変化を調べるため、GAD67-GFPマウスを使用して解析を行ったところ、有意差は認めなかったものの、抑制性神経に強くpCREBの発現を認めた。この現象はCCIモデルでも同様に確認された。このことから、SNL術後早期には、抑制性の神経細胞の活動性が低下することで、興奮性細胞の相対的な活性化が生じ、その結果疼痛閾値が低下するのではないかと推察された。その後、in vivoパッチを立ち上げることに成功し、マウス右後肢を筆で刺激することによってEPSCが増強する範囲を記録した。

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  • 幼若脳組織の神経活動に対する麻酔薬の作用の解明

    2010年4月 - 2013年3月

    日本学術振興会  科学研究費補助金 

    安藤 富男

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    資金種別:競争的資金

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  • 難治性疼痛に対する脊髄刺激鎮痛法の作用点の解明 -中枢か脊髄か-

    2010年4月 - 2013年3月

    日本学術振興会  科学研究費補助金 

    紙谷 義孝

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    担当区分:研究代表者  資金種別:競争的資金

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  • 疼痛が記憶学習に及ぼす影響の、行動学的及び中枢神経系での組織学・生理学的検討

    2010年4月 - 2013年3月

    日本学術振興会  科学研究費補助金 

    小川 賢一

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    資金種別:競争的資金

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  • Sema3Aの疼通抑制作用における神経成長因子の関与の解明

    2009年4月 - 2012年3月

    日本学術振興会  科学研究費補助金 

    紙谷 義孝

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    担当区分:研究代表者  資金種別:競争的資金

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  • 麻酔薬の幼弱脳神経毒性に対するエリスロポイエチンの予防効果

    2009年4月 - 2012年3月

    日本学術振興会  科学研究費補助金 

    越後 憲之

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    資金種別:競争的資金

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  • 神経因性疼痛における神経ガイダンス因子の多角的アプローチによる分子標的の解明

    2007年4月 - 2010年3月

    日本学術振興会  科学研究費補助金 

    紙谷 義孝

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    担当区分:研究代表者  資金種別:競争的資金

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  • 神経保護因子としてのエリスロポイエチンの新しい作用メカニズムの解明

    2007年4月 - 2010年3月

    日本学術振興会  科学研究費補助金 

    安藤 富男

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    資金種別:競争的資金

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  • Mechanisms of spinal cord stimulation for attenuation of neuropathic pain in rodent model

    2007年

    Basic Science Research Program 

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    資金種別:競争的資金

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  • 麻酔薬の中脳ドパミンニューロンに対する影響と耽溺性との関連の解明

    2006年4月 - 2008年3月

    日本学術振興会  科学研究費補助金 

    小川 賢一

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    資金種別:競争的資金

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  • Effects of anesthetics on midbrain dopaminergic neurons

    2006年

    Basic Science Research Program 

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    資金種別:競争的資金

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  • Roles of neuronal guidance factors for neuropathic pain

    2006年

    Basic Science Research Program 

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    資金種別:競争的資金

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  • 揮発性麻酔薬の神経細胞のフリーラジカルに対する作用の解明

    2005年4月 - 2007年3月

    日本学術振興会  科学研究費補助金 

    紙谷 義孝

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    担当区分:研究代表者  資金種別:競争的資金

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  • 神経因性疼痛時の脊髄内神経回路リモデリングにおける神経ガイダンス因子の役割

    2004年4月 - 2007年3月

    日本学術振興会  科学研究費補助金 

    山田 芳嗣

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    資金種別:競争的資金

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  • G蛋白質連関型ドーパ受容体候補の機能解析と新規低分子活性物質の構造決定

    2004年4月 - 2006年3月

    日本学術振興会  科学研究費補助金 

    五嶋 良郎

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    資金種別:競争的資金

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  • グルタミン酸受容体のゲート機構の解析及び同機構に及ぼす麻酔薬の影響

    2001年4月 - 2004年3月

    日本学術振興会  特別研究員奨励費 

    紙谷 義孝

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    担当区分:研究代表者  資金種別:競争的資金

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