Neuronal Excitatory Action of GABA on the Pelvic Ganglia

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.