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A selective adenosine antagonist (8-cyclopentyl-1,3-dipropylxanthine) eliminates both neuromuscular depression and the action of exogenous adenosine by an effect on A1 receptors

RS Redman and EM Silinsky

Department of Pharmacology, Northwestern University, Chicago, Illinois 60611.

The effect of 8-cyclopentyl-1,3-dipropylxanthine (DPCPX), a selective A1 adenosine receptor antagonist, was studied at frog motor nerve endings in the hope of determining whether the inhibitory effects of exogenous or endogenous adenosine on neurotransmitter release are mediated by an A1 receptor or the postulated prejunctional "A3 receptor." These putative A3 receptors have been reported to have a lower affinity for DPCPX (>> 1 nM) than A1 receptors (50-190 pM) and have been linked to changes in Ca2+ translocation. The affinity of DPCPX as an antagonist of exogenous adenosine at frog motor nerve endings was calculated by using the Schild equation and found to range from 25 to 200 pM (n = 12). These values are consistent with the presence of A1 receptors. The effect of endogenous adenosine as a mediator of prejunctional neuromuscular depression produced by repetitive nerve impulses was fully reversed by 100 pM DPCPX. Neither prejunctional neuromuscular depression produced by endogenous or exogenous adenosine nor the reversal of depression by DPCPX was associated with changes in nerve terminal Ca2+ currents. The results demonstrate that endogenous or exogenous adenosine mediates neuromuscular depression in the frog, via an A1 receptor.

Volume 44, Issue 4, pp. 835-840, 10/01/1993
Copyright © 1993 by American Society for Pharmacology and Experimental Therapeutics




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Copyright © 1993 by the American Society for Pharmacology and Experimental Therapeutics