Modification of nicotinic ganglionic transmission by muscarinic slow postsynaptic potentials in the in vitro rabbit superior cervical ganglion.

The influence of slow muscarinic postsynaptic potentials, i.e., the s-IPSP and s-EPSP, on synaptic transmission mediated through nicotinic receptors was studied in the superior cervical ganglion of the rabbit. Postganglionic spikes and synaptic potentials were elicited by delivery of conditioning and test stimulus pulses to afferent fibers. When paired stimulus volleys were separated by brief intervals (20-100 msec) or long intervals (1,000-8,000 msec), the population spike elicited by the test stimulus was larger in amplitude than that elicited by the conditioning volley. When paired stimulus volleys were separated by 250-500 msec, the amplitude of the population spike elicited by the test volley was smaller than that elicited by the conditioning stimulus. Gallamine, which selectively blocks the s-IPSP, reduced the suppression of the test spike which occurred when stimulus IPIs ranged between 250-500 msec. Pirenzepine, which selectively blocks the s-EPSP, reduced the late facilitation of test postganglionic spikes which occurred with stimulus IPIs greater than 1,000 msec. The non-selective muscarinic antagonist QNB, produced changes in postganglionic spike amplitude that were similar to the combined effects of gallamine and pirenzepine. The evidence indicates that the s-IPSP and s-EPSP modified the excitability state of the ganglionic neurons and subsequent synaptic transmission that was mediated through nicotinic receptors.