Actions of cholecystokinin and norepinephrine on vagal inputs to ganglion cells in guinea pig gallbladder.

Previous studies have demonstrated that all guinea pig gallbladder neurons receive nicotinic synaptic input and that cholecystokinin (CCK) and norepinephrine have presynaptic facilitory and inhibitory effects, respectively, on these fast synaptic events. The current study was undertaken to determine the sources of the cholinergic terminals that provide nicotinic input to gallbladder neurons. To stimulate potential extrinsic inputs to gallbladder neurons, a stimulating electrode was placed on the nerve bundles that pass along the cystic duct. Stimulation of these nerves elicited fast excitatory postsynaptic potentials (EPSPs) in gallbladder neurons that were sensitive to hexamethonium, facilitated by CCK, and inhibited by norepinephrine. After vagotomy, most neurons (14 of 18) did not exhibit any nicotinic input. However, some neurons (3 of 18) did exhibit fast EPSPs in response to fiber tract stimulation, but not cystic nerve stimulation, indicating that interganglionic communication does exist amongst gallbladder neurons. These results demonstrate that the vagus nerves provide the major nicotinic input to gallbladder neurons. Furthermore, these data suggest that vagal terminals within gallbladder are a site of neurohormonal modulation of gallbladder ganglionic output by CCK, norepinephrine, and possibly other compounds.