RT Journal Article SR Electronic T1 THE ACTIONS OF SEVERAL GANGLION BLOCKING AGENTS ON THE POSTGANGLIONIC DISCHARGE INDUCED BY DIISOPROPYL PHOSPHOROFLUORIDATE (DFP) IN SYMPATHETIC GANGLIA JF Journal of Pharmacology and Experimental Therapeutics JO J Pharmacol Exp Ther FD American Society for Pharmacology and Experimental Therapeutics SP 45 OP 53 VO 135 IS 1 A1 Volle, Robert L. YR 1962 UL http://jpet.aspetjournals.org/content/135/1/45.abstract AB 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.