GABAC receptors mediate slow membrane potentials in neurons of the rat major pelvic ganglia.

Effects of gamma-aminobutyric acid (GABA) on the neuronal membrane of the rat major pelvic ganglia (MPG) were studied using intracellular recording techniques, in vitro. Application of GABA (100 microM) to MPG neurons induced a depolarization (GABAd) associated with a decreased membrane input resistance and a slow hyperpolarization (s-GABAh) associated with an increased membrane input resistance. The GABA depolarization had two phases, a fast depolarization (f-GABAd) and a subsequent slow depolarization (s-GABAd). Bicuculline (60 microM) blocked the f-GABAd but not the s-GABAd and s-GABAh. Picrotoxin (100 microM) blocked all the GABA responses. Imidazole-4-acetic acid (I4AA, 100 microM), a GABAc receptor antagonist, depressed the s-GABAd and s-GABAh, but did not block the f-GABAd. Cis-4-aminocrotonic acid (CACA), a GABAc receptor agonist, produced a depolarization followed by a hyperpolarization in MPG neurons. I4AA (100 microM) depressed the CACA-induced responses. It was concluded that GABAA receptors mediate the f-GABAd and that GABAc receptors mediate the s-GABAd and s-GABAh, in neurons of the rat MPG.