CHOLINERGIC TRANSMISSION IN PANCREATIC GANGLIA OF THE CAT

Although there is considerable evidence indicating the existence of im portant cholinergic neural regulation of pancreatic function, very lit tle is known about the action of acetylcholine on pancreatic ganglion neurons. The present study was undertaken to determine the effect of p ressure microejection of acetylcholine and muscarine on ganglion cell excitability of the cat pancreas. Recordings were made in vitro from g anglion neurons located in the head region of the pancreas. Acetylchol ine evoked a fast- and a slow-developing membrane depolarization in th e majority of neurons tested. A decrease in membrane input resistance accompanied the fast depolarizing response, whereas an increase in inp ut resistance accompanied the slow depolarizing response. The fast res ponse was mimicked by 1,1-dimethyl-4-phenylpiperazinium iodide and nic otine and antagonized by hexamethonium. The slow depolarizing response was mimicked by muscarine and antagonized by atropine and pirenzepine . The dependence of the slow depolarization on extracellular K+ and th e distinct voltage dependence of the slow depolarization suggest that activation of muscarinic receptors was due to inactivation of I-M. The slow excitatory postsynaptic potential and associated increase in exc itability evoked by repetitive nerve stimulation was partially choline rgic dependent in the majority of neurons tested. It was concluded tha t cholinergic transmission in cat pancreatic ganglia involves nicotini c and M(1) receptors that mediate fast and slow synaptic transmission, respectively, and that activation of M(1) receptors modifies the outp ut firing frequency.