EFFECT OF NALOXONE AND PROLONGED PREGANGLIONIC STIMULATION ON NONCHOLINERGIC TRANSMISSION IN THE SUPERIOR CERVICAL-GANGLION OF THE CAT

In cats anesthetized with sodium pentobarbital, a supramaximal 40-Hz, 30-s train to the cervical sympathetic trunk, during block of ganglionic cholinergic transmission with hexamethonium and scopolamine, produced a delayed, slow, small amplitude contraction of the nictitating membrane that persisted for several minutes after the end of the stimulus train. The post-stimulus component of the response was due to afterdischarge of the ganglion cells, since section of post-ganglionic axons at the end of the train resulted in elimination of this component. The amplitude of the slow nictitating membrane response was enhanced in a dose-dependent manner by i.v. injection of naloxone. The enhancement was detectable at a dose as low as 1 μg/kg and was maximal at 10 μg/kg. During continuous preganglionic stimulation at 40 Hz, the amplitude of the slow nicittating membrane response reached a peak in 2-4 min and then faded with time until it became undetectable. Time for 90% decay was 82 ± 5 min (n = 18). The nicittating membrane response to postganglionic nerve stimulation was not modified by prolonged preganglionic stimulation. In three cats, the cervical sympathetic trunk was split into two bundles and one bundle was stimulated continuously at 40 Hz until the slow response disappeared. At this time stimulation of the unconditioned bundle evoked a slow response of normal appearance. This suggest that the process underlying the fade involves only the conditioned axons. Recovery from the fade was slow, the response approaching control by 24 h poststimulus. In contrast, the nicittating membrane response mediated by ganglionic nicotinic transmission was of amplitude similar to control within the 1st min after the end of a 2-h period of continuous 40 Hz stimulation. The fade and recovery of the slow response may be the consequence of presynaptic events and reflect the exhaustion followed by slow replenishment of the releasable stores of the noncholinergic transmitter. The enhancement of the slow response by naloxone suggests that an inhibitory noncholinergic transmitter, presumably an opioid, is also released by the preganglionic axon terminals.