摘要

Presynaptic inhibition is a major mechanism for regulating synaptic transmission in the CNS and adenosine inhibits Ca2+ currents (I-Ca) to reduce transmitter release at several synapses. Rod photoreceptors possess L-type Ca2+ channels that regulate the release of L-glutamate. In the retina, adenosine is released in the dark when L-glutamate release is maximal. We tested whether adenosine inhibits I-Ca and intracellular Ca2+ increases in rod photoreceptors in retinal slice and isolated cell preparations. Adenosine inhibited both I-Ca and the [Ca2+](i) increase evoked by depolarization in a dose-dependent manner with similar to25% inhibition at 50 muM. An A(2)-selective agonist, (N-6-[2-(3,5-dimethoxyphenyl)-2-(2-methylphenyl)- ethyl]adenosine) (DPMA), but not the A(1)- or A(3)-selective agonists, (R)-N-6-(1-methyl-2-phenylethyl)adenosine and N-6-2-(4-aminophenyl)ethyladenosine, also inhibited I-Ca and depolarization-induced [Ca2+](i) increases. An inhibitor of protein kinase A (PKA), Rp-cAMPS, blocked the effects of DPMA on both I-Ca and the depolarization-evoked [Ca2+](i) increase in rods. The results suggest that activation of A(2) receptors stimulates PKA to inhibit L-type Ca2+ channels in rods resulting in a decreased Ca2+ influx that should suppress glutamate release.

  • 出版日期2002-1