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Journal of Pharmacology And Experimental Therapeutics, Vol. 162, Issue 1, 30-37, 1968
Copyright © 1968 by American Society for Pharmacology and Experimental Therapeutics


GANGLIONIC ACTIONS OF agr,aacgr-BIS-(DIMETHYLAMMONIUMACET-ALDEHYDE DIETHYLACETAL)-DIACETYLBIPHENYL DIBROMIDE (DMAE)

JORGE JARAMILLO 1

1 Department of Pharmacology, Tulane University School of Medicine, New Orleans, Louisiana

Electrophysiologic studies of the effects of agr,aacgr-bis-(dimethylammoniumacetaldehyde diethylacetal)rgr,rgr-diacetylbiphenyl dibromide (DMAE) were made on the superior cervical ganglion of the cat. The direct effects observed after the intraarterial administra-tion of small doses of DMAE consisted only of ganglionic depolarization. Larger doses produced depolarization and blockade of transmission. The blockade of transmission had characteristics of the classical ganglion blocking agents. Since no changes in afterpotentials, suggestive of modifications on the polarization state of the ganglion, were observed after DMAE, depolarization is believed to arise from ganglionic sites other than those involved in the transmission process. Marked changes in the ganglionic effects of the nicotinic stimulants were observed after DMAE. The postganglionic firing and ganglionic depolarization and hyperpolarization produced by tetramethylammonium (TMA) and dimethylphenylpiperazinium (DMPP) were considerably depressed or totally abolished by DMAE. The block of transmission and concomitant hyperpolarization observed during the second phase of blockade by TMA and DMPP were completely antagonized by doses of DMAE that did not affect the spike amplitude. The early block of transmission produced by DMPP and TMA was either unmodified or increased after DMAE in doses producing antagonism of the late block. It is concluded that DMAE possesses an antinicotinic effect like that of hexamethonium. The ability to suppress the excitatory effects of the nicotinic stimulants without affecting the spike amplitude makes DMAE a valuable tool for the understanding of the DMPP-or TMA-induced late block of transmission.

Submitted on December 6, 1967
Accepted on March 12, 1968







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Copyright © 1968 by the American Society for Pharmacology and Experimental Therapeutics.