ACTIONS OF CHOLECYSTOKININ AND NOREPINEPHRINE ON VAGAL INPUTS TO GANGLION-CELLS IN GUINEA-PIG GALLBLADDER

Previous studies have demonstrated that all guinea pig gallbladder neu rons receive nicotinic synaptic input and that cholecystokinin (CCK) a nd norepinephrine have presynaptic facilitory and inhibitory effects, respectively, on these fast synaptic events. The current study was und ertaken to determine the sources of the cholinergic terminals that pro vide nicotinic input to gallbladder neurons. To stimulate potential ex trinsic inputs to gallbladder neurons, a stimulating electrode was pla ced on the nerve bundles that pass along the cystic duct. Stimulation of these nerves elicited fast excitatory postsynaptic potentials (EPSP s) in gallbladder neurons that were sensitive to hexamethonium, facili tated by CCK, and inhibited by norepinephrine. After vagotomy, most ne urons (14 of 18) did not exhibit any nicotinic input. However, some ne urons (3 of 18) did exhibit fast EPSPs in response to fiber tract stim ulation, but not cystic nerve stimulation, indicating that intergangli onic communication does exist amongst gallbladder neurons. These resul ts demonstrate that the vagus nerves provide the major nicotinic input to gallbladder neurons. Furthermore, these data suggest that vagal te rminals within gallbladder are a site of neurohormonal modulation of g allbladder ganglionic output by CCK, norepinephrine, and possibly othe r compounds.