RELATIONSHIPS BETWEEN DRUG-EVOKED POTENTIALS AND TRANSMISSION IN A SYMPATHETIC GANGLION

¹ Department of Pharmacology, School of Medicine, Tulane University, New Orleans, Louisiana

A study was made of the effects of N-ethylmaleimide (NEM) on transmission, neurogenically evoked synaptic potential, drug-induced surface potentials and drug-induced firing in the superior cervical ganglion of the cat. Whereas a small dose of NEM enhanced the ganglionic action potential, the synaptic potential and the firing produced by acetylcholine (ACh) or tetramethylammonium chloride (TMA), it depressed the depolarization evoked by ACh or TMA and the hyperpolarization evoked by methacholine and norepinephrine. Moreover, NEM antagonized the block of transmission produced by ACh, TMA, methacholine and norepinephrine. The latter findings indicate that NEM stabilized the ganglion cells insofar as drug-induced surface potentials are concerned. The opposite actions of NEM on the synaptic potential and drug-induced depolarization can be explained by postulating 1) that NEM promoted an increase in ACh release from the nerve terminals in amounts adequate to overcome depression by NEM of the ganglion cell, 2) that injected ACh had ganglionic actions different from those of endogenous ACh or 3) that the depolarization of the ganglia evoked by ACh arose from extrajunctional cholinoceptive sites. The depression of ACh-induced depolarization at a time when firing was enhanced suggests a differential effect of NEM on the chemosensitive and spike-generating sites within the ganglion cells.