THE A(1) AGONIST CCPA REDUCED BISOXONOL-MONITORED MEMBRANE-POTENTIAL DEPOLARIZATION ELICITED BY HIGH K+ IN CEREBROCORTICAL NERVE-ENDINGS

In this study the effect of the A(1) agonist 2-chloro-N-6-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 mu M) caused a dose-dependent decrease of high K+- and veratridine-induced membrane depolarization. This decrease was counteracted by the A(1)-specific antagonist 1,3-dipropyl-8-cyclopentylxanthine (DPCPX) (30-100 mu M). On the contrary, the A, 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 interfere with the lowering effect exerted by CCPA (100 mu M) on K+-elicited membrane depolarization. Finally, the A(2) 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 A(1) receptors.