Involvement of protein kinase C in the Ca2+-dependent vesicular release of GABA from central and enteric neurons of the guinea pig.

The involvement of protein kinase C (PKC) in the release of endogenous gamma-aminobutyric acid (GABA) was studied using slices of deep cerebellar nucleus and strips of small intestine from the guinea pig. 12-O-tetradecanoylphorbol 13-acetate (TPA), but not 4 alpha-phorbol-12,13-didecanoate (4 alpha-PDD), potentiated the high K+-evoked release of GABA from both preparations in the presence of tetrodotoxin. Ouabain evoked the release of GABA from both preparations, and this release was not altered by TPA. Therefore, the activation of protein kinase C potentiates the Ca2+-dependent vesicular release of GABA from nerve terminals of the central and enteric GABAergic neurons of the guinea pig.