Abstract

The effect of cholecystokinin octapeptide (CCK8) on neurons of inferior mesenteric ganglion of the guinea pig was examined with intracellular microelectrodes. CCK8 nonsulfated pressure ejected from micropipettes resulted in a depolarization of 95% of neurons tested. The ED50 for depolarization was 1.1 +/- S.D. 0.5 pmol. The maximum depolarization averaged 9.3 mV (+/- S.D. 6.1 mV) and lasted for 99.7 sec (+/- S.D. 14.6 sec). In 73% of the cells the depolarization was associated with either an increase or a decrease in the cell input resistance; the remainder depolarized without a change in input resistance. In those cells in which the input resistance decreased during depolarization (59% of cells tested), the null potential was -36.3 +/- 9.3 mV. In those cells in which the input resistance increased during depolarization (20% of cells tested), the null potential was -103 +/- 6 mV). In those cells that depolarized without a change in input resistance (21% of cells tested) the null potential was -90.4 +/- 2.3 mV. At an equal dose, the sulfated form of CCK8 resulted in a depolarization that was 47% (+/- 26%) smaller in amplitude and 27% (+/- 21%) shorter in duration than the depolarization produced by the nonsulfated form of CCK8. The effects of both forms of CCK8 were not abolished in low calcium-high magnesium, suggesting a direct action on the postsynaptic membrane. Application of CCK8 at intervals less than 10 min resulted in marked desensitization of the response. Desensitization to CCK8 reduced by 52% (+/- 9%) the amplitude of the nerve-evoked slow excitatory postsynaptic potential in 67% of cells in which it was tested.(ABSTRACT TRUNCATED AT 250 WORDS)