MODULATION OF CA2-TERMINALS( CHANNELS BY ACTIVATION OF ADENOSINE A(1)RECEPTORS IN RAT STRIATAL GLUTAMATERGIC NERVE)

We determined that activation of adenosine A(1) receptors in striatal synaptosomes with 100 nM N-6-cyclopentyladenosine (CPA) inhibited both the release of endogenous glutamate and the increase of intracellular free Ca2+ concentration ([Ca2+](i)), due to 4-aminopyridine (4-AP) st imulation, by 28 and 19%, respectively. Furthermore, CPA enhanced the inhibition of endogenous glutamate release due to omega-conotoxin GVIA (omega-Cgtx GVIA), omega-Cgtx MVIIC or omega-Cgtx GVIA plus omega-Cgt x MVIIC. Similar effects were observed in the [Ca2+](i) signal. The in hibitory effects of CPA and omega-Cgtx GVIA were additive, but the eff ects of CPA and omega-Cgtx MVIIC were only partially additive. These r esults suggest that P/Q-type Ca2+ channels and other type(s) of Ca2+ c hannel(s), coupled to glutamate release, are inhibited subsequently to activation of adenosine A(1) receptors. (C) 1996 Elsevier Science Ire land Ltd.