Neuronal Excitatory Action of GABA on the Pelvic Ganglia.
- Author:
Seung Bae GILL
1
;
Seung Kyu CHA
;
Dae Ran KIM
;
Sang Gun JANG
;
Yeun Kyeu JANG
;
In Deok KONG
Author Information
1. Department of Neurosurgery, Gangneung Asan Hospital, University of Ulsan College of Medicine, Gangneung, Korea.
- Publication Type:Original Article
- Keywords:
Major pelvic ganglia;
GABA;
GABAA receptor
- MeSH:
Animals;
Autonomic Nervous System;
Bicuculline;
Central Nervous System;
Chloride Channels;
gamma-Aminobutyric Acid*;
Ganglia*;
Humans;
Male;
Membrane Potentials;
Membranes;
Neurons*;
Neurotransmitter Agents;
Niflumic Acid;
Patch-Clamp Techniques;
Prostate;
Rats
- From:Journal of Korean Neurosurgical Society
2004;36(2):145-149
- CountryRepublic of Korea
- Language:Korean
-
Abstract:
OBJECTIVE: In the central nervous system, gamma-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 (100micrometer) 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 (10micrometer, 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 GABA-induced depolarizations were largely blocked by bicuculline(10micrometer, n=6), but not by DIDS(50micrometer, 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.
