MECHANISMS INVOLVED IN GANGLIONIC BLOCKADE INDUCED BY TETRAMETHYLAMMONIUM

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

Tetramethylammonium (TMA)-induced block of transmission in the superior cervical ganglion of the cat was characterized by a sequential pattern of 1) blockade associated with ganglionic depolarization (TMA-early block), 2) recovery from block during the falling phase of depolarization and 3) the reappearance of ganglionic blockade associated with ganglionic hyperpolarization (TMA-late block). That the late block of transmission produced by TMA differed from that evoked by hexamethonium was indicated by 1) a rise in the ganglion demarcation potential, 2) changes in the contour of the evoked ganglionic action potential consistent with hyperpolarization and 3) an increase in acetylcholine- (ACh-) induced depolarization at a time when postganglionic firing produced by ACh was suppressed. Both the hyperpolarization and late-occurring block produced by TMA were antagonized by repetitive preganglionic stimulation, pilocarpine, 2-diethoxyphosphenylthioethyldimethylamine acid oxalate (217A0) or ouabain. Ouabain also antagonized the positive afterpotential following a single ganglionic spike and posttetanic hyperpolarization, but had not effect on ganglionic blockade produced by hexamethonium, methacholine or epinephrine. Pilocarpine, 217A0 and tetanus slightly enhanced or had no effect on block occurring during TMA- induced depolarization. Ouabain usually did not alter TMA-induced early block and depolarization. The findings with ouabain suggest that the late block and hyperpolarization produced by TMA were caused by a mechanism similar to that responsible for the positive afterpotential following the ganglionic spike.

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