THE TRANSMISSION OF IMPULSES THROUGH A SYMPATHETIC GANGLION

Abstract
The resemblances between sympathetic ganglia and motor plates of skeletal muscles are reviewed, and the methods here used[long dash]study of the superior cervical ganglion (s.c.g.) having a natural blood supply and influencing the nictitating membrane) (n.m.)[long dash]are descr. Evidence is presented as to relative doses of acetylcholine (a-ch.) which produce stimulant and depressant effects on the s.cg. Prostigmin (used instead of eserine) may have a depressant action on the ganglion, but it may clearly potentiate the responses to maximal single shocks applied to the preganglionic (pre-g.) fibers. It has no direct effect on the postganglionic (post-g.) fibers or n.m. Given shortly before tetanic stimulation of pre-g. fibers prostigmin cuts short the contraction and turns it into relaxation; as minutes pass the depressant action gradually disappears. The relaxation is attributed to excess of a-ch., preserved from prompt destruction by prostigmin. If injected after tetanic stimulation of pre-g. fibers has failed to maintain the n.m. in full contraction, prostigmin causes an increase of contraction. If the lower contraction resulted from "fatigue" (i.e., insufficient a-ch. to activate some ganglion cells), the increase is explicable as a preservation of a-ch. until more cells are activated. Injection of a-ch. during the fatigue phase has an effect similar to that produced by prostigmin, and can be explained on the same basis; injected at the start of tetanic stimulation, a-ch., like prostigmin, quickly interrupts contraction and induces relaxation. Again the action, like that of prostigmin, is attributable to a depressant excess of a-ch. at this phase. Either a-ch. or prostigmin has a decurarizing action on the ganglion. In explanation, curare may be regarded as raising the threshold of excitation of the ganglion cells, so that the fatigue effect is magnified (i.e., the level of contraction falls); a-ch., by supplying an extra quantity, and prostigmin, by protecting from destruction the a-ch. which is naturally produced, raise the stimulus above the raised threshold. A brief tetanus, introduced in a series of maximal single shocks, causes the succeeding contractions to be much higher than those which preceded. Probably the tetanus releases in the gangliaan adjuvant (perhaps K) of a-ch., which results in repetitive discharges from single pre-g. volleys. In the discussion the bearing of these observations on the chemical theory of synaptic transmission is considered.

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