Modulation of Ca2+ channels by activation of adenosine A1 receptors in rat striatal glutamatergic nerve terminals

Abstract

We determined that activation of adenosine A1 receptors in striatal synaptosomes with 100 nM N6-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) stimulation, 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-Cgtx MVIIC. Similar effects were observed in the [Ca2+]i signal. The inhibitory effects of CPA and omega-Cgtx GVIA were additive, but the effects of CPA and omega-Cgtx MVIIC were only partially additive. These results suggest that P/Q-type Ca2+ channels and other type(s) of Ca2+ channel(s), coupled to glutamate release, are inhibited subsequently to activation of adenosine A1 receptors.