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Journal of Korean Neurosurgical Society 2004;36(2): 145-149.
Neuronal Excitatory Action of GABA on the Pelvic Ganglia.
Seung Bae Gill, Seung Kyu Cha, Dae Ran Kim, Sang Gun Jang, Yeun Kyeu Jang, In Deok Kong
1Department of Neurosurgery, Gangneung Asan Hospital, University of Ulsan College of Medicine, Gangneung, Korea.
2Department of Physiology, Yonsei University Wonju College of Medicine, Wonju, Korea. kong@wonju.yonsei.ac.kr
3Department of Neurosurgery, KunKuk University College of Medicine, Seoul, Korea.
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.
Key Words: Major pelvic ganglia; GABA; GABAA receptor
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