Pre- and postsynaptic components of nicotinic long-term potentiation in the superior cervical ganglion of the cat.

1. In anesthetized, atropine-treated cats we measured the acetylcholine (ACh) release into the venous effluent of the superior cervical ganglion (SCG) and the nictitating membrane (NM) contraction evoked by a 2-Hz, 20-s test train to the ipsilateral cervical sympathetic trunk (CST). We also measured NM contraction produced by injection of ACh (50 micrograms) or 1,1-dimethyl-4-phenylpiperazinium (DMPP, 5 micrograms) into the arterial supply of the ipsilateral SCG. 2. After a 10- to 30-s, 40-Hz conditioning train to CST these responses were all potentiated. The potentiation of the NM response evoked by the test train or by the exogenous agonists was long lasting (90% decay in 64 +/- 10 min, mean +/- SE, for the train-evoked response; 42 +/- 9 min for the response to injected ACh; 61 +/- 18 min for the response to injected DMPP), whereas the potentiation of the ACh release lasted only for 9 min. 3. On the assumption that ACh and DMPP injected into the ganglionic arterial supply acted postsynaptically, these data suggest that the main mechanism of the long-term potentiation (LTP) of nicotinic transmission in SCG is an increase in postsynaptic responsiveness. Because the response to KCl (250 micrograms) injected into the ganglionic arterial supply was not potentiated after the conditioning train, a posttrain increase in excitability of the postsynaptic membrane is not likely to be the cause of the postsynaptic increased responsiveness to ACh and DMPP.(ABSTRACT TRUNCATED AT 250 WORDS)