Cholinergic transmission in pancreatic ganglia of the cat

Although there is considerable evidence indicating the existence of important cholinergic neural regulation of pancreatic function, very little is known about the action of acetylcholine on pancreatic ganglion neurons. The present study was undertaken to determine the effect of pressure microejection of acetylcholine and muscarine on ganglion cell excitability of the cat pancreas. Recordings were made in vitro from ganglion neurons located in the head region of the pancreas. Acetylcholine evoked a fast- and a slow- developing membrane depolarization in the majority of neurons tested. A decrease in membrane input resistance accompanied the fast depolarizing response, whereas an increase in input resistance accompanied the slow depolarizing response. The fast response was mimicked by 1,1-dimethyl-4- phenylpiperazinium iodide and nicotine 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 the 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 excitability evoked by repetitive nerve stimulation was partially cholinergic dependent in the majority of neurons tested. It was concluded that cholinergic transmission in cat pancreatic ganglia involves nicotinic and M₁ receptors that mediate fast and slow synaptic transmission, respectively, and that activation of M₁ receptors modifies the output firing frequency.