FURTHER LOCALIZATION AND ANALYSIS OF ADRENERGIC SYNAPTIC INHIBITION

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Abstract
By using the action potentials in the postganglionic nerves as an index of synaptic activity, one of the authors found in 1939 that intravenous epinephrine, in doses from 5 y upwards, inhibited transmission in the superior cervical sympathetic ganglion of the cat. The pres -ent work, using the same technique, shows that the inhibitory action of epinephrine can be demonstrated in all sympathetic ganglia. In the inferior mesenteric ganglia, some fibers run right through without synapsing. The potentials of these non-synapsing fibers are recorded simultaneously with those of the postsynaptic fibers and it is demonstrated that epinephrine blocks synaptic transmission without affecting nerve conduction. "Continuous records of the synaptic action of intravenously injected epinephrine show that the inhibition comes on without preliminary stimulation and that it is independent of circulatory effects. A "post-inhibitory" facilitation is described during the recovery from epinephrine inhibition. This is shown to be a non-specific phenomenon which can be reproduced by inducing simple ischemia of the ganglia. The post-inhibitory facilitation is attributed in part to the ganglionic ischemia which epinephrine produces. The specific epinephrine inhibition and the nonspecific facilitation are thought to develop concurrently[long dash]though independently[long dash] but the latter at a slower rate, due to the slowly developing effects of ischemia, so that it appears as a late phenomenon. The synaptic excitatory action of epinephrine described by Bulbring and Burn is shown to be a non-specific post-inhibi-tory phenomenon in expts. in which the initial primary inhibition is missed because of the late recording. The generalized inhibitory action of epinephrine at adrenergic neuro-neuronal inhibitory junctions is interpreted as opposed and reciprocating with the cholinergic excitatory mechanism at sympathetic synapses and as a potential physiological mechanism that could participate in synaptic transmission and constitute the basis for a""self-limiting homeostatic mechanism." In circulatory shock it does not appear possible that the synaptic action of epinephrine can play any but a protective role.

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