No 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 (10M) induced slow depolarizations in approximately 70% of tested cells. PACAP-induced depolarizations were approximately 10mV in the peak amplitude, and their durations were approximately 10 min. The slow depolarizations were accompanied by a decrease in membrane conductance (g m ) at the initial phase and an increase in g m at the peak phase. Membrane input resistance increased by ‫%2.2ע8.41‬ (mean‫ע‬S.E., max.) of the resting value at the initial phase and decreased by ‫%3.4ע8.03‬ (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 4Hz in the initial phase during the slow depolarizations. The decrease in g m was probably produced by an inhibition of calcium conductance and an inhibition of slow Ca ‫ם2‬-activated K ‫ם‬ channels, while the increase in g m 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.

Angiotensin II acts as an excitatory neurotransmitter of the sympathetic ganglia. In the parasympathetic neurons, however, angiotensin II (angio II)-induced responses have not been recorded. In this study, we investigated the effects of angio II in the hamster submandibular ganglion (SMG) neurons using a intracellular recording technique. Approximately 70% of these ganglion cells responded with persistent depolarization (3-6 mV, 5-9min) at a concentration of 10M. The angio II-induced depolarizations were caused by the combination of an increase in Na ‫ם‬ conductance and a decrease in K ‫ם‬conductance. An involvement of K ‫ם‬ channels such as M channels and SK channels in the electrogenesis mechanism was suggested by an inhibitory effect of Ba ‫ם2‬ ion on the component of the increased membrane input resistance during the angio II-induced depolarization. In addition, the angio II-induced depolarizations were mediated through angio II type I (AT 1 ) receptors. Thus angio II is probably a neurotransmitter that increases their excitability in most of the neurons in parasympathetic ganglia.