골반 신경절에 대한 GABA의 신경 흥분성 작용

Objective : In the central nervous system, γ-aminobutyric acid (GABA) is well known to act as an inhibitory neurotransmitter by hyperpolarizing postsynaptic neurons through gating GABA-activated Cl- channels. To date, however, the functional roles of GABA remain unclear in the autonomic nervous syst...

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Published inJournal of Korean Neurosurgical Society pp. 145 - 149
Main Authors 길승배, 차승규, 김대란, 장상근, 장연규, 공인덕
Format Journal Article
LanguageKorean
Published 대한신경외과학회 01.08.2004
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ISSN2005-3711
1598-7876

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Summary:Objective : In the central nervous system, γ-aminobutyric acid (GABA) is well known to act as an inhibitory neurotransmitter by hyperpolarizing postsynaptic neurons through gating GABA-activated Cl- channels. To date, however, the functional roles of GABA remain unclear in the autonomic nervous system. In the present study, we characterize GABA-activated Cl- currents in the neurons of major pelvic ganglia (MPG). Methods : MPG neurons, located on the lateral surfaces of the prostate gland, from male rats were enzymatically dissociated. Ionic currents were recorded using whole-cell variant patch-clamp technique. Membrane potential was recorded under current clamp mode. Current traces were filterd at 2kHz by using 4-pole Bassel filter in the amplifier. Results : Application of GABA (100㎛) induced inward currents in the neurons, with holding potentials being maintained below the Cl- equilibrium potential (ECl). The GABA response was concentration-dependent and its reversal potential was close to the theoretical ECl. The GABA-induced Cl- currents were largely blocked by bicuculline (10㎛, n=5), a GABAA receptor antagonist, but were not affected by 9-AC and niflumic acid, chloride channel blockers. GABA also produced significant membrane depolarization (19mV, n=28). As in the case of the Cl- currents, the GABAinduced depolarizations were largely blocked by bicuculline(10㎛, n=6), but not by DIDS(50㎛, n=4), another chloride channel blocker. Conclusion : The data suggest that GABAergic roles may be due to it's activation of excitatory GABAA receptors, which are expressed in MPG neurons. KCI Citation Count: 0
Bibliography:G704-001031.2004.36.2.012
http://kmbase.medric.or.kr/Main.aspx?d=KMBASE&m=VIEW&i=1001920040360020145
ISSN:2005-3711
1598-7876