SITE OF THE INHIBITORY-ACTION OF ENDOGENOUS OPIOIDS IN THE SUPERIOR CERVICAL-GANGLION OF THE CAT

A low-frequency stimulus train to the preganglionic input inhibits syn aptic transmission in the superior cervical ganglion (SCG) of the cat. The inhibition is blocked by naloxone as well as by selective antagon ists at mu and delta opiate receptors, which suggests that the mediato r is an endogenous opioid [27,29]. Exogenous opioid peptides, includin g methionine-enkephalin (Met-Enk), which is present in preganglionic a xons of the SCG, inhibit ganglionic transmission by a naloxone-sensiti ve mechanism. In the present study we test, in the anesthetized cat, w hether the naloxone-sensitive synaptic inhibition is mediated by a pre - and/or post-synaptic mechanism. As a test of presynaptic inhibition, we measured the acetylcholine (ACh) released by preganglionic stimula tion into the venous effluent of the perfused SCG. As a test of post-s ynaptic inhibition, we measured the effect of a preganglionic conditio ning train on the ganglion cell firing evoked by ganglion-stimulant dr ugs injected into the arterial supply of the ganglion. In presence of naloxone (3 mu M), which blocked the synaptic inhibition, the amount o f ACh released by stimulated preganglionic axons did not change. Thus, the endogenous opioid which mediates the naloxone-sensitive inhibitio n does not act by depressing ACh release. In contrast, the ganglion ce ll firing evoked by ganglion-stimulant drugs was markedly depressed by a conditioning train, and naloxone blocked the depression, which sugg ests that the endogenous mediator of the naloxone-sensitive inhibition acts postsynaptically to decrease the excitability of ganglion cells. Exogenous Met-Enk depressed both ACh release by preganglionic stimula tion and the firing of ganglion cells evoked by ganglion-stimulant dru gs. These findings suggest that although opiate receptors in the cat S CG are present at both pre- and post-synaptic sites, under the conditi ons of the present experiment the naloxone-sensitive, synaptically med iated inhibition is mediated exclusively by activation of post-synapti c opiate receptors.