PACAP-induced depolarizations in hamster submandibular ganglion neurons.

Abstract

In this study, we have investigated the effects of pituitary adenylate cyclase-activating polypeptide (PACAP) on in vitro hamster submandibular ganglion neurons using the conventional intracellular recording technique. PACAP (10 microM) induced slow depolarizations in approximately 70% of tested cells. PACAP-induced depolarizations were approximately 10 mV in the peak amplitude, and their durations were approximately 10 min. The slow depolarizations were accompanied by a decrease in membrane conductance (gm) at the initial phase and an increase in gm at the peak phase. Membrane input resistance increased by 14.8 +/- 2.2% (mean +/- S.E., max.) of the resting value at the initial phase and decreased by 30.8 +/- 4.3% (max.) at the peak phase. Anodal break spikes were elicited at the initial phase during PACAP-induced depolarization. In one neuron, anodal break spikes were elicited at the peak. Spikes which followed the anodal break spike were also elicited at 4 Hz in the initial phase during the slow depolarizations. The decrease in gm was probably produced by an inhibition of calcium conductance and an inhibition of slow Ca(2+)-activated K+ channels, while the increase in gm might have been produced by an activation of nonselective cation channels. The slow depolarizations by PACAP might be mediated by a membrane-delimited signal transduction cascade involving G protein in the submandibular ganglion neurons.