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Journal of Pharmacology And Experimental Therapeutics, Vol. 135, Issue 1, 45-53, 1962
Copyright © 1962 by American Society for Pharmacology and Experimental Therapeutics


THE ACTIONS OF SEVERAL GANGLION BLOCKING AGENTS ON THE POSTGANGLIONIC DISCHARGE INDUCED BY DIISOPROPYL PHOSPHOROFLUORIDATE (DFP) IN SYMPATHETIC GANGLIA

Robert L. Volle 1

1 Department of Pharmacology, Schools of Medicine, University of Pennsylvania, Philadelphia, Pennsylvania

The effects of various ganglionic blocking agents on three types of ganglionic activity were compared: viz., postganglionic action potentials evoked by stimulation of the preganglionic nerve, persistent asynchronous postganglionic discharge of resting ganglia following the administration of diisopropyl phosphorofluoridate (DFP), and the postganglionic responses to injected acetylcholine (ACh). Tetraethylammonium ion, in doses which blocked completely the evoked action potential and the responses to injected ACh, first enhanced then depressed the DFP-induced discharge. Hexamethonium abolished both the postganglionic spike and the ganglionic responses to ACh but had little effect on the discharge. d-Tubocurarine, although producing a complete blockade of the spike and responses to ACh, had a stimulatory effect only on the DFP-induced discimarge. Mecamylamine, like d-tubocurarine, enhanced the discharge. On the other hand, atropine and procaine, in doses which had no demonstrable effect on the postganglionic spike or responses to ACh, blocked completely the DFP-induced discharge. It was reported also that atropine in doses which blocked completely the DFP-induced discharge had no effect on the after-discharge evoked by brief tetanic preganglionic stimulation.

The findings are interpreted as an indication of time existence of different mechanisms of transmission within the superior cervical ganglion. Several possible explanations of these observations are discussed.

The enhancenment by tetraethylammonium ion, d-tubocurarine, and mecamylamine of the postganglionic discharge is attributed to an action of these agents of the presynaptic nerve terminals.

Submitted on June 16, 1961







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Copyright © 1962 by the American Society for Pharmacology and Experimental Therapeutics.