Misc - HONMOU Osamu

脳動脈瘤患者の PKD1 遺伝子解析

脳血管攣縮   15   0-0  1999

The delayed depolarization in rat cutaneous afferent axons is reduced following nerve transection and ligation, but not crush: Implications for injury-induced axonal Na+ channel reorganization

J Sakai, O Honmou, JD Kocsis, K Hashi

MUSCLE & NERVE   21 ( 8 ) 1040 - 1047  1998.08

DOI

B-17)中枢神経系脱髄疾患への髄鞘形成細胞移植療法における免疫応答 : MHCノックアウトマウスを用いた主要組織適合抗原の検討（北日本脳神経外科連合会 第22回学術集会）

加藤 孝顕, 本望 修, 酒井 淳, 上出 廷治, 端 和夫

新潟医学会雑誌 ( 新潟医学会 )  112 ( 8 ) 498 - 498  1998.08

CiNii

B-16)神経損傷及び再生時のslow Na＾+ channel発現の制御（北日本脳神経外科連合会 第22回学術集会）

野中 雅, 本望 修, 酒井 淳, 端 和夫

新潟医学会雑誌 ( 新潟医学会 )  112 ( 8 ) 498 - 498  1998.08

CiNii

B-18)神経幹細胞の脳および培養海馬への移植（北日本脳神経外科連合会 第22回学術集会）

酒井 淳, 本望 修, 加藤 孝顕, 端 和夫

新潟医学会雑誌 ( 新潟医学会 )  112 ( 8 ) 498 - 498  1998.08

CiNii

B-19)てんかんに対する遺伝子療法（北日本脳神経外科連合会 第22回学術集会）

本望 修, 端 和夫

新潟医学会雑誌 ( 新潟医学会 )  112 ( 8 ) 498 - 499  1998.08

CiNii

Transplantation of the genetically-engineering neural stem cell

HONMOU Osamu, KATO Takaaki, HASHI Kazuo

神経組織の成長・再生・移植   10 ( 1 ) 61 - 62  1998.06

CiNii

Transplantation of the cultured human olfactory ensheathing cell to the rat demyelinated spinal cord

KATO Takaaki, HONMOU Osamu, HASHI Kazuo

神経組織の成長・再生・移植   10 ( 1 ) 23 - 24  1998.06

CiNii

DNA diagnosis in the NF2 gene

Tumor Research   32   33 - 39  1998

B-57)遺伝子組み換え細胞移植による脱髄疾患の治療 : 機能回復の評価と臨床応用への可能性(北日本脳神経外科連合会 第21回学術集会)

本望 修, 端 和夫

新潟医学会雑誌 ( 新潟医学会 )  111 ( 9 ) 602 - 602  1997.09

CiNii

B-56)神経損傷及び再生時におけるNa^+ channel発現の変化(北日本脳神経外科連合会 第21回学術集会)

酒井 淳, 本望 修, 端 和夫

新潟医学会雑誌 ( 新潟医学会 )  111 ( 9 ) 602 - 602  1997.09

CiNii

中枢性脱髄疾患に対する遺伝子組み換えシュワン細胞の移植—ラット脊髄後索脱髄モデルを用いた軸索伝導機能回復の検討

外科治療   77   622 - 623  1997

Restoration of normal conduction properties in demyelinated spinal cord axons in the adult rat by transplantation of exogenous Schwann cells

O Honmou, PA Felts, SG Waxman, JD Kocsis

JOURNAL OF NEUROSCIENCE   16 ( 10 ) 3199 - 3208  1996.05

グリア細胞移植による髄鞘形成: 先天性脱髄モデル myelin-deficient rat を用いた軸索伝導機能回復の検討

神経免疫   9   279 - 281  1996

THE ANTICONVULSANT GABAPENTIN ENHANCES PROMOTED RELEASE OF GABA IN HIPPOCAMPUS - A FIELD POTENTIAL ANALYSIS

O HONMOU, AA OYELESE, JD KOCSIS

BRAIN RESEARCH ( ELSEVIER SCIENCE BV )  692 ( 1-2 ) 273 - 277  1995.09

Article, review, commentary, editorial, etc. (scientific journal)  

　View Summary

The mechanism of action of the recently developed anticonvulsant gabapentin (GBP) used for treatment of partial seizures [12] is largely unknown. Rat hippocampal slices were maintained in vitro and the effects of microapplication of nipecotic acid (NPA), which promotes the release and blocks uptake of GABA, on the synaptically-evoked population excitatory postsynaptic potential (EPSP) were assessed before and after 1 h bath application of GBP. GBP treatment did not alter the population EPSP amplitude to paired or multiple stimuli, but nearly doubled the shunting effects of NPA on the EPSP with no effect on the presynaptic volley. The NPA-induced shunting of the EPSP was bicuculline-sensitive, indicating its mediation by GABA(A) receptor activation. These results suggest that GBP may increase free GABA levels in hippocampal cells, the release of which may be enhanced under conditions of promoted GABA release. Moreover, the study presents a methodology to electrophysiologically assess relative free GABA levels using field potential analysis in the adult rat brain.

DOI PubMed CiNii

NOREPINEPHRINE MODULATES EXCITABILITY OF NEONATAL RAT OPTIC NERVES THROUGH CALCIUM-MEDIATED MECHANISMS

O HONMOU, W YOUNG

NEUROSCIENCE ( PERGAMON-ELSEVIER SCIENCE LTD )  65 ( 1 ) 241 - 251  1995.03

　View Summary

We report that norepinephrine markedly increases excitability of neonatal rat optic nerves. To investigate the mechanisms of the norepinephrine-induced excitability increase, we studied isolated optic nerves from 42 neonatal (< three days old) and five adult (> three months old) Long-Evan's hooded rats. Norepinephrine (10(-6), 10(-5) and 10(-4) M) rapidly and reversibly increased the amplitudes (mean +/- S.D.: 3.5 +/- 1.7%, 12.1 +/- 2.8% and 35.6 +/- 8.4%) of compound action potentials elicited by submaximal stimulation of neonatal optic nerves. The beta-1 adrenoceptor antagonist atenolol (10(-5) M) blocked the norepinephrine-induced increase in excitability but the alpha antagonist phentolamine (10(-5) M) did not. The beta agonist isoproterenol (10(-5) and 10(-4) M) increased response amplitudes (8.7 +/- 4.1% and 25.8 +/- 4.6%) but the alpha-1 agonist methoxamine and alpha-2 agonist clonidine did not. The beta antagonist propranolol blocked the isoproterenol effect. Replacing Ca2+ with Mg2+ or adding 0.8 mM of Cd2+ reversibly blocked the norepinephrine effects. Extracellular K+ concentrations did not change in optic nerves during norepinephrine application. Blockade of K+ channels with apamin (10(-6) M) or tetraethylammonium (10(-3) M) did not prevent the excitatory effects of norepinephrine. Adult rat optic nerves were insensitive to both norepinephrine (10(-4) M) and isoproterenol (10(-4) M). Our results indicate that norepinephrine increases neonatal optic axonal excitability through Ca2+-dependent mechanisms. The data suggest that the adrenoceptors are situated on the axons, that the excitability changes are not due to changes in extracellular K+ concentration or K+ channels sensitive to apamin or tetraethylammonium. The sensitivity of rat optic nerves to norepinephrine declined with age. Axonal adrenoceptors may play a role in optic axonal development and injury.

DOI PubMed CiNii

GABAPENTIN POTENTIATES THE CONDUCTANCE INCREASE INDUCED BY NIPECOTIC ACID IN CA1 PYRAMIDAL NEURONS IN-VITRO

O HONMOU, JD KOCSIS, GB RICHERSON

EPILEPSY RESEARCH ( ELSEVIER SCIENCE BV )  20 ( 3 ) 193 - 202  1995.03

　View Summary

The anticonvulsant gabapentin (1-(aminomethyl)cyclohexane acetic acid) has been found to be effective for treatment of partial seizures, but the mechanism of action is unknown. Recent evidence from the rat optic nerve suggests that gabapentin may enhance promoted release of GABA, which is thought to be due to reverse operation of the GABA transporter. We have used whole-cell patch clamp recordings from CA1 pyramidal neurons in hippocampal slices to directly measure currents induced by nipecotic acid (NPA) during exposure to gabapentin. Under control conditions, pressure microejection of NPA increased whole-cell conductance with a reversal potential equal to the chloride equilibrium potential. This response was mimicked by GABA application, and blocked by bicuculline. The response to NPA was also present after blockade of synaptic transmission in the presence of calcium-free solution. These results are consistent with NPA promoting nonvesicular release of GABA from neighboring neurons or glia via reverse operation of the GABA uptake system, which then activated GABA, receptors on the recorded neurons. In control solution, the response to NPA slowly decreased over 45 min to approximately 50% of the initial response, consistent with GABA, receptor 'rundown'. However, in the presence of gabapentin there was a slow increase in the response, reaching approximately 170% of the control level after 45 min of gabapentin exposure. These results demonstrate that gabapentin enhances the promoted release of GABA by more than three-fold. The potentiation of the NPA response may be due to gabapentin increasing cytosolic GABA in neighboring cells via a delayed metabolic effect, and would have the functional effect of increasing neuronal inhibition during periods of hyperexcitability.

Traumatic injury of spinal axons, in The Axon; structure, function and pathophysiology

Oxford University Press    1995

DELAYED DEPOLARIZATION AND SLOW SODIUM CURRENTS IN CUTANEOUS AFFERENTS

O HONMOU, DA UTZSCHNEIDER, MA RIZZO, CM BOWE, SG WAXMAN, JD KOCSIS

JOURNAL OF NEUROPHYSIOLOGY   71 ( 5 ) 1627 - 1637  1994.05

GABAPENTIN INCREASES GABA-INDUCED DEPOLARIZATION IN RAT NEONATAL OPTIC-NERVE

JD KOCSIS, O HONMOU

NEUROSCIENCE LETTERS   169 ( 1-2 ) 181 - 184  1994.03