The A1 agonist CCPA reduced bisoxonol-monitored membrane potential depolarization elicited by high K+ in cerebrocortical nerve endings.

In this study the effect of the A1 agonist 2-chloro-N6-cyclopentyladenosine (CCPA) on bis(1,3-diethylthiobarbituric acid)trimethine oxonol (bisoxonol)-monitored membrane potential in cerebrocortical nerve endings was evaluated. CCPA (30, 100 and 300 microM) caused a dose-dependent decrease of high K(+)- and veratridine-induced membrane depolarization. This decrease was counteracted by the A1-specific antagonist 1,3-dipropyl-8-cyclopentylxanthine (DPCPX) (30-100 microM). On the contrary, the A2 receptor antagonist 9-chloro-2-(2-furanyl)-5,6-dihydro-1,2,4-triazolol-[1,5-c]quinazol ine-5- imine (CGS 15943) was unable to interfere with the lowering effect exerted by CCPA (100 microM) on K(+)-elicited membrane depolarization. Finally, the A2 receptor agonist 2-[p-(2-carboxyethyl)phenethylamine]-5'-N-ethylcarboxamidoadenosine (CGS 21680) did not induce any modification of K(+)-induced membrane depolarization. The results of the present study suggest that K(+)-induced membrane depolarization in cerebrocortical brain nerve endings may be modulated by A1 receptors.