Faculty Profiles - BABA Hiroshsi

Papers - BABA Hiroshsi

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The effect of PGE2 on rat spinal dorsal horn neurons Reviewed

Ataka T, Wakai A, Okamoto M, Baba H

The Joural of Functional Diagnosis of the Spinal Cord 25 ( 1 ) 13 - 17 2003

炎症性疼痛の脊髄内メカニズム－特にPGE2の役割について－ Reviewed

生駒美穂, 馬場洋

麻酔 52 S34-46 2003

脊髄におけるノルアドレナリン作動性下行性痛覚抑制の機序 Reviewed

岡本学, 馬場洋

臨床麻酔 27 ( 8 ) 1251 - 1262 2003

Technical developments of the ultra-fine flexible fiberscope for diagnosis of spinal and cerebroventricular diseases Reviewed

Shimoji K, Tomita M, Tobita T, Yamakura T, Okamoto M, Ataka T, Baba H

The Journal of Functional Diagnosis of the Spinal Cord 25 ( 1 ) 1 - 8 2003

Gabapentin - Actions on adult superficial dorsal horn neurons Reviewed

KA Moore, H Baba, CJ Woolf

NEUROPHARMACOLOGY 43 ( 7 ) 1077 - 1081 2002.12

Language：English Publishing type：Research paper (scientific journal) Publisher：PERGAMON-ELSEVIER SCIENCE LTD

Despite identification of GABA(B) receptors with gb1a-gb2 composition and the alpha2delta calcium channel subunit as putative molecular targets for gabapentin (GBP), its cellular mechanism of action has remained elusive. Therefore, we have used an in vitro spinal cord slice preparation to study the effects of GBP on lamina 11 neurons. The frequency and amplitude of spontaneous EPSCs and IPSCs were unaffected by GBP, suggesting presynaptic neurotransmitter release is not regulated. Direct modulation of postsynaptic membrane excitability is also unlikely since the level of holding current required to maintain neurons at -70, 0 and +45 mV was unaffected by GBP. Effects on excitatory and inhibitory synaptic transmission were variable across the population. Primary afferent-evoked fast glutamatergic EPSCs were unaffected by GBP, while evoked NMDA receptor-mediated EPSCs and IPSCs were variably affected. In contrast, GBP enhanced responses to bath applied NMDA in 71% of neurons. Thus, in adult rat dorsal horn, synaptic and extrasynaptic NMDA receptors may be differentially regulated by GBP perhaps due to differences in subunit composition. (C) 2002 Elsevier Science Ltd. All rights reserved.

File： Moore(Neuropharmacology).pdf

DOI： 10.1016/S0028-3908(02)00226-5

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Ischemic preconditioning is capable of inducing mitochondrial tolerance in the rat brain Reviewed

RZ Zhan, H Fujihara, H Baba, T Yamakura, K Shimoji

ANESTHESIOLOGY 97 ( 4 ) 896 - 901 2002.10

Language：English Publishing type：Research paper (scientific journal) Publisher：LIPPINCOTT WILLIAMS & WILKINS

Background: Preconditioning to ischemia is a phenomenon whereby a brief episode of sublethal ischemia and other non-lethal stressors produce protection against a subsequent detrimental ischemic insult. As mitochondrial dysfunction is related to necrotic and apoptotic neuronal death after cerebral ischemia, the authors examined if ischemic preconditioning is capable of inducing mitochondrial tolerance.
Methods: Forebrain ischemia was induced by bilateral common carotid artery occlusion with simultaneous hypotension for 8 min in Wistar rats (275-300 g). A 3-min ischemic episode performed 48 It before the 8-min ischemia was used for preconditioning. The extents of hippocampal CA1 neuronal damage were evaluated 7 days after reperfusion by neuro-specific nuclear protein immunostaining. Brain mitochondria were isolated 48 It after animals were subjected to the sham operation or the 3-min conditioning ischemia. Loss of cytochrome c from mitochondria after cerebral ischemia in vivo and after exposure of brain mitochondria to calcium in vitro was used as an indication of mitochondrial dysfunction.
Results: Results showed that ischemic preconditioning induced by a 3-min ischemic episode dramatically reduced the loss of hippocampal CA1 neurons resulting from a subsequent 8-min ischemia 7 days after reperfusion, and this protection was associated with a preservation of mitochondrial cytochrome c as examined after early reperfusion. Exposure of isolated brain mitochondria to calcium produced a dose-dependent increase in cytochrome c release either at 30degreesC or at 37degreesC. Compared with those animals receiving only sham operation, cytochrome c release caused by 100 muM calcium was significantly reduced in conditioned animals.
Conclusion: Regarding the importance of mitochondrial dysfunction in mediating ischemic neuronal death, the above results indicate that mitochondria may serve as end-effecting organelles to ischemic preconditioning.

File： Zhan(Anesthesiology,2002),.pdf

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Successful use of laryngeal mask airway for a patient with tracheal stenosis with tracheobronchopathia osteochondroplastica Reviewed

H Ishii, H Fujihara, T Ataka, H Baba, T Yamakura, T Tobita, K Taga, K Shimoji

ANESTHESIA AND ANALGESIA 95 ( 3 ) 781 - 782 2002.9

Partial peripheral nerve injury promotes a selective loss of GABAergic inhibition in the superficial dorsal horn of the spinal cord Reviewed

KA Moore, T Kohno, LA Karchewski, J Scholz, H Baba, CJ Woolf

JOURNAL OF NEUROSCIENCE 22 ( 15 ) 6724 - 6731 2002.8

Language：English Publishing type：Research paper (scientific journal) Publisher：SOC NEUROSCIENCE

To clarify whether inhibitory transmission in the superficial dorsal horn of the spinal cord is reduced after peripheral nerve injury, we have studied synaptic transmission in lamina II neurons of an isolated adult rat spinal cord slice preparation after complete sciatic nerve transection (SNT), chronic constriction injury (CCI), or spared nerve injury (SNI). Fast excitatory transmission remains intact after all three types of nerve injury. In contrast, primary afferent-evoked IPSCs are substantially reduced in incidence, magnitude, and duration after the two partial nerve injuries, CCI and SNI, but not SNT. Pharmacologically isolated GABA(A) receptor-mediated IPSCs are decreased in the two partial nerve injury models compared with naive animals. An analysis of unitary IPSCs suggests that presynaptic GABA release is reduced after CCI and SNI. Partial nerve injury also decreases dorsal horn levels of the GABA synthesizing enzyme glutamic acid decarboxylase (GAD) 65 kDa ipsilateral to the injury and induces neuronal apoptosis, detected by terminal deoxynucleotidyl transferase-mediated biotinylated UTP nick end labeling staining in identified neurons. Both of these mechanisms could reduce presynaptic GABA levels and promote a functional loss of GABAergic transmission in the superficial dorsal horn.

File： Moore (JNS).pdf

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Propofol enhances GABAA receptor-mediated presynaptic inhibition in human spinal cord Reviewed

Miyako Shimizu, Tomohiro Yamakura, Toshiyuki Tobita, Manabu Okamoto, Toyofumi Ataka, Hideyoshi Fujihara, Kiichiro Taga, Koki Shimoji, Hiroshi Baba

NeuroReport 13 ( 3 ) 357 - 360 2002.3

Authorship：Last author,　Corresponding author Language：English Publishing type：Research paper (scientific journal) Publisher：Lippincott Williams and Wilkins

Although the function of somatodendritic GABAA receptors is augmented by propofol, it is not known whether presynaptic GABAA receptor function is similarly affected. In the present study, we examined the action of propofol on the second positive wave (P2 component) of segmental spinal cord evoked potentials (seg SCEPs), which is believed to reflect GABAA receptor-mediated presynaptic inhibition of primary afferent terminals and can be recorded from spinal epidural space in man. In all seven patients tested while undergoing scoliosis surgery, a clinical dose of propofol (1 mg/kg, i.v.) significantly augmented the P2 component of seg SCEPs evoked by ulner nerve stimulation. We conclude that propofol enhances GABAA receptor-mediated presynaptic inhibition at primary afferent terminals in human spinal cord. © 2002 Lippincott Williams &amp
Wilkins.

DOI： 10.1097/00001756-200203040-00021

塩酸メキシレチンが有効であった肢端紅痛症の1症例 Reviewed

和栗紀子, 安宅豊史, 冨田美佐雄, 馬場洋

ペインクリニック 23 ( 9 ) 1314 - 1315 2002

上位胸部持続硬膜外ブロック中断後、瞳孔散大による一過性の視力低下を呈した1症例 Reviewed

安宅豊史, 和栗紀子, 冨田美佐緒, 馬場洋

ペインクリニック 23 ( 11 ) 1577 - 1578 2002

Sublethal cerebral ischemia inhibits caspase-3 activation induced by subsequent prolonged ischemia in the C57black/Crj6 strain mouse Reviewed

SH Qi, RZ Zhan, CR Wu, H Fujihara, T Yamakura, H Baba, K Taga, K Shimoji

NEUROSCIENCE LETTERS 315 ( 3 ) 133 - 136 2001.11

Language：English Publishing type：Research paper (scientific journal) Publisher：ELSEVIER SCI IRELAND LTD

Caspase-3 activation has been implicated in ischemic neuronal death. In the present study, we examined if cerebral ischemic tolerance induced by sublethal ischemia is associated with an attenuation of caspase-3 activation in a mouse forebrain ischemia model. Forebrain ischemia in C57Black/Crj6 strain mice was induced by bilateral common carotid artery occlusion (BCCAO) for 18 min. Two episodes of 6-min ischemia were carried out as preconditioning 48 and 72 h before the 18-min BCCAO. Caspase-3-like activity was determined by fluorescently monitoring the release of amino-4-methylcoumarin from N-acetyl-Asp-Glu-Val-Asp-7-amino-4-methylcoumarin in the striatal protein extracts at 4, 24, and 72 h after reperfusion. The results showed that the ischemic preconditioning significantly attenuated caspase-3 activation at 4, 24, and 72 h after reperfusion, and reduced neuronal loss caused by the 18-min ischemia as examined on the 7th day after reperfusion. The present results suggest that the neuroprotection achieved by ischemic preconditioning is related to an attenuation of caspase-3 activation. (C) 2001 Elsevier Science Ltd. All rights reserved.

DOI： 10.1016/S0304-3940(01)02368-0

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The placement of the epidural catheter at the predicted site by electrical stimulation test Reviewed

K Hayatsu, M Tomita, H Fujihara, H Baba, T Yamakura, K Taga, K Shimoji

ANESTHESIA AND ANALGESIA 93 ( 4 ) 1035 - 1039 2001.10

Language：English Publishing type：Research paper (scientific journal) Publisher：LIPPINCOTT WILLIAMS & WILKINS

More accurate segmental and sagittal positioning of the epidural catheter tip is required for the success of continuous epidural analgesia, spinal cord monitoring, and percutaneous epidural spinal cord stimulation. We examined the usefulness of an electrical stimulation test for verifying the proper placement of the epidural catheter tip at the predicted site in the posterior epidural space by using a locally developed epidural catheter with electrodes at its tip. The test included the observation of segmental bilateral muscle twitches and the patient's report of feeling in the region stimulated by moving the epidural catheter electrode back and forth and changing the direction of the bevel of the Tuohy needle. The success rate of midline placement at the required spinal segment was significantly more frequent (99%; P < 0.001) in the group (n = 289) receiving the electrical stimulation test compared with the group (n = 277) not receiving the test (success rate 57%). The results indicate the usefulness of this method. We concluded that the electrical stimulation test is effective for verifying the proper placement of the catheter electrode tip.

File： Hayatsu(A&A,2001).pdf

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The paired homeodomain protein DRG11 is required for the projection of cutaneous sensory afferent fibers to the dorsal spinal cord Reviewed

ZF Chen, S Rebelo, F White, AB Malmberg, H Baba, D Lima, CJ Woolf, AI Basbaum, DJ Anderson

NEURON 31 ( 1 ) 59 - 73 2001.7

Language：English Publishing type：Research paper (scientific journal) Publisher：CELL PRESS

Cutaneous sensory neurons that detect noxious stimuli project to the dorsal horn of the spinal cord, while those innervating muscle stretch receptors project to the ventral horn. DRG11, a paired homeodomain transcription factor, is expressed in both the developing dorsal horn and in sensory neurons, but not in the ventral spinal cord. Mouse embryos deficient in DRG11 display abnormalities in the spatio-temporal patterning of cutaneous sensory afferent fiber projections to the dorsal, but not the ventral spinal cord, as well as defects in dorsal horn morphogenesis. These early developmental abnormalities lead, in adults, to significantly attenuated sensitivity to noxious stimuli. In contrast, locomotion and sensori-motor functions appear normal. Drg11 is thus required for the formation of spatio-temporally appropriate projections from nociceptive sensory neurons to their central targets in the dorsal horn of the spinal cord.

File： Chen(Neuron).pdf

DOI： 10.1016/S0896-6273(01)00341-5

Functional reorganization of sensory pathways in the rat spinal dorsal horn following peripheral nerve injury Reviewed

M Okamoto, H Baba, PA Goldstein, H Higashi, K Shimoji, M Yoshimura

JOURNAL OF PHYSIOLOGY-LONDON 532 ( 1 ) 241 - 250 2001.4

Language：English Publishing type：Research paper (scientific journal) Publisher：WILEY-BLACKWELL

1. Functional reorganization of sensory pathways in the rat spinal dorsal horn following sciatic nerve transection was examined using spinal cord slices with an attached dorsal root. Slices were obtained from animals whose sciatic nerve had been transected 2-4 weeks previously and compared to sham-operated controls.
2. Whole-cell recordings from substantia gelatinosa neurones in sham-operated rats, to which nociceptive information was preferentially transmitted, revealed that dorsal root stimulation sufficient to activate A delta afferent fibres evoked a mono- and/or polysynaptic EPSC in 111 of 131 (similar to 85%) neurones. This is in contrast to the response following A beta fibre stimulation? where monosynaptic EPSCs were observed in 2 of 131 (similar to2%) neurones and polysynaptic EPSCs were observed in 18 of 131 (similar to 14%) neurones.
3. In sciatic nerve-transected rats, however, a polysynaptic EPSC following stimulation of A beta afferents was elicited in 30 of 37 (81%) neurones and a monosynaptic EPSC evoked by A beta afferent stimulation was detected in a subset of neurones (4 of 37, similar to 11%).
4. These observations suggest that, following sciatic nerve transection, large myelinated A beta afferent fibres establish synaptic contact with interneurones and transmit innocuous information to substantia gelatinosa. This functional reorganization of the sensory circuitry may constitute an underlying mechanism, at least in part, for sensory abnormalities following peripheral nerve injuries.

File： Okamoto(JP,2001).pdf

DOI： 10.1111/j.1469-7793.2001.0241g.x

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Direct activation of rat spinal dorsal horn neurons by prostaglandin E2 Reviewed

H Baba, T Kohno, KA Moore, CJ Woolf

JOURNAL OF NEUROSCIENCE 21 ( 5 ) 1750 - 1756 2001.3

Authorship：Lead author,　Corresponding author Language：English Publishing type：Research paper (scientific journal) Publisher：SOC NEUROSCIENCE

Whole-cell patch-clamp and intracellular recording techniques have been used to study the action of prostaglandin E2 (PGE2) on neurons in adult rat transverse spinal cord slices. Bath-applied PGE2 (1-20 muM) induced an inward current or membrane depolarization in the majority of deep dorsal horn neurons (laminas III-VI; 83 of 139 cells), but only in a minority of lamina II neurons (6 of 53 cells). PGE2 alone never elicited spontaneous action potentials; however, it did convert subthreshold EPSPs to suprathreshold, leading to action potential generation. PGE2-induced inward currents were unaffected by perfusion with either a Ca2+-free/high Mg2+ (5 mM) solution or tetrodotoxin (1 muM), indicating a direct postsynaptic action. Both 17-phenyl trinor prostaglandin E2 (an EP1 agonist) and sulprostone (an EP3 agonist) had little effect on membrane current, whereas butaprost methyl ester (an EP2 agonist) mimicked the effect of PGE2. Depolarizing responses to PGE2 were associated with a decrease in input resistance, and the amplitude of inward current was decreased as the holding potential was depolarized. PGE2-induced inward currents were reduced by substitution of extracellular Na+ with N-methyl-D-glucamine and inhibited by flufenamic acid (50-200 muM), which is compatible with activation of a nonselective cation channel. These results suggest that PGE2, acting via an EP2-like receptor, directly depolarizes spinal neurons. Moreover, these findings imply an involvement of spinal cord-generated prostanoids in modulating sensory processing through an alteration in dorsal horn neuronal excitability.

File： Baba(PGE2,JNS,2001).pdf

DOI： 10.1523/JNEUROSCI.21-05-01750.2001

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麻酔とGABA Reviewed

馬場洋, 下地恒毅

臨床麻酔 25 ( 3 ) 468 - 476 2001

Preemptive analgesia by intravenous low-dose ketamine and epidural morphine in gastrectomy - A randomized double-blind study Reviewed

S Aida, T Yamakura, H Baba, K Taga, S Fukuda, K Shimoji

ANESTHESIOLOGY 92 ( 6 ) 1624 - 1630 2000.6

Language：English Publishing type：Research paper (scientific journal) Publisher：LIPPINCOTT WILLIAMS & WILKINS

Background: Morphine and ketamine may prevent central sensitization during surgery and result in preemptive analgesia. The reliability of preemptive analgesia, however, is controversial.
Methods: Gastrectomy patients were given preemptive analgesia consisting of epidural morphine, intravenous low-dose ketamine, and combinations of these in a randomized, double-blind manner. Postsurgical pain intensity was rated by a visual analog scale, a categoric pain evaluation, and cumulative morphine consumption.
Results: Preemptive analgesia by epidural morphine and by Intravenous low-dose ketamine were significantly effective but not definitive. With epidural morphine, a significant reduction in visual analog scale scores at rest was observed at 24 and 48 h, and morphine consumption was significantly lower at 6 and It h, compared with control values. With intravenous ketamine, visual analog scale scores at rest and morphine consumption were significantly lower at 6, 12, 24, and 48 h than those in control subjects. The combination of epidural morphine and intravenous ketamine provided definitive preemptive analgesia: Visual analog scale scores at rest and morphine consumption were significantly the lowest at 6, 12, 24, and 48 h, and the visual analog scale score during movement and the categoric pain score also were significantly the lowest among the groups.
Conclusion: The results suggest that for definitive preemptive analgesia, blockade of opioid and N-methyl-D-aspartate receptors is necessary for upper abdominal surgery such as gastrectomy; singly, either treatment provided significant, but not definitive, postsurgical pain relief. Epidural morphine may affect the spinal cord segmentally, whereas intravenous ketamine may block brain stem sensitization ain the vagus nerve during upper abdominal surgery.

File： Aida(Anesthesiology,2000).pdf

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Norepinephrine facilitates inhibitory transmission in substantia gelatinosa of adult rat spinal cord (Part 1) - Effects on axon terminals of GABAergic and glycinergic neurons Reviewed

H Baba, K Shimoji, M Yoshimura

ANESTHESIOLOGY 92 ( 2 ) 473 - 484 2000.2

Language：English Publishing type：Research paper (scientific journal) Publisher：LIPPINCOTT WILLIAMS & WILKINS

Background: The activation of descending norepinephrine containing fibers from the brain stem inhibits nociceptive transmission at the spinal level. How these descending noradrenergic pathways exert the analgesic effect is not understood fully. Membrane hyperpolarization of substantia gelatinosa (Rexed lamina II) neurons by the activation of alpha(2) receptors may account for depression of pain transmission. In addition, it is possible that norepinephrine affects transmitter release in the substantia gelatinosa.
Methods: Adult male Sprague-Dawley rats (9-10 weeks of age, 250-300 g) were used in this study. Transverse spinal cord slices were cut from the isolated lumbar cord. The blind whole-cell patch-clamp technique was used to record from neurons. The effects of norepinephrine on the frequency and amplitude of miniature excitatory and inhibitory postsynaptic currents were evaluated.
Results: In the majority of substantia gelatinosa neurons tested, norepinephrine (10-100 mu M) dose-dependently increased the frequency of gamma-aminobutyric acid (GABA)-ergic and glycinergic miniature inhibitory postsynaptic currents; miniature excitatory postsynaptic currents were unaffected, This augmentation was mimicked by an alpha(1)-receptor agonist, phenylephrine (10-60 mu M), and inhibited by alpha(1)-receptor antagonists prazosin (0.5 mu M) and 2-(2,6-dimethoxyphenoxyethyl) aminomethyl-1,4-benzodioxane (0.5 mu M). Neither postsynaptic responsiveness to exogenously applied GABA and glycine nor the kinetics of GABAergic and glycinergic inhibitory postsynaptic currents were affected by norepinephrine.
Conclusion: These results suggest that norepinephrine enhances inhibitory synaptic transmission in the substantia gelatinosa through activation of presynaptic alpha(1) receptors, thus providing a mechanism underlying the clinical use of of, agonists with local anesthetics in spinal anesthesia.

File： NApart1(Anesthesiology2000).pdf

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Silent NMDA receptor-mediated synapses are developmentally regulated in the dorsal horn of the rat spinal cord Reviewed

H Baba, TP Doubell, KA Moore, CJ Woolf

JOURNAL OF NEUROPHYSIOLOGY 83 ( 2 ) 955 - 962 2000.2

Language：English Publishing type：Research paper (scientific journal) Publisher：AMER PHYSIOLOGICAL SOC

Silent NMDA receptor-mediated synapses are developmentally regulated in the dorsal horn of the rat spinal cord. J. Neurophysiol. 83: 955-962, 2000. In vitro whole cell patch-clamp recording techniques were utilized to study silent pure-N-methyl-D-aspartate (NMDA) receptor-mediated synaptic responses in lamina II (substantia gelatinosa, SG) and lamina III of the spinal dorsal hem. To clarify whether these synapses are present in the adult and contribute to neuropathic pain, transverse lumbar spinal cord slices were prepared from neonatal, naive adult and adult sciatic nerve transected rats. In neonatal rats, pure-NMDA receptor-mediated excitatory postsynaptic currents (EPSCs) were elicited in SG neurons either by focal intraspinal stimulation (n = 15 of 20 neurons) or focal stimulation of the dorsal root (n = 2 of 7 neurons). In contrast, in slices from naive adult rats, no silent pure-NMDA EPSCs were recorded in SG neurons following focal intraspinal stimulation (n = 27), and only one pure-NMDA EPSC was observed in lamina III (n = 23). Furthermore, in rats with chronic sciatic nerve transection, pure-NMDA EPSCs were elicited by focal intraspinal stimulation in only 2 of 45 SG neurons. Although a large increase in A beta fiber evoked mixed alpha-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid (AMPA) and NMDA receptor-mediated synapses was detected after sciatic nerve injury, A beta fiber-mediated pure-NMDA EPSCs were not evoked in SG neurons by dorsal root stimulation. Pure-NMDA receptor-mediated EPSCs are therefore a transient, developmentally regulated phenomenon, and, although they may have a role in synaptic refinement in the immature dorsal horn, they are unlikely to be involved in receptive field plasticity in the adult.

File： jn.2000.83.2.955.pdf

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Papers - BABA Hiroshsi