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 μM) 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 μM). On the contrary, the A₂ receptor antagonist 9-chloro-2-(2-furanyl)-5,6-dihydro-1,2,4-triazolol-[1,5-c]quinazoline-5-imine (CGS 15943) was unable to interface with the lowering effect exerted by CCPA (100 μM) on K⁺-elicited membrane depolarization. Finally, the A₂ receptor agonist 2-[p-(2-carboxyl-ethyl)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.