Abstract
The hippocampal GABAergic system is assumed not to be a target for purine modulation. We have now confirmed that neither adenosine A 1 and A 3 receptor nor nucleotide P 2 or P 4 receptor activation modified the K +-evoked [ 3H]GABA release from hippocampal synaptosomes. However, activation of adenosine A 2A receptors with CGS 21680 (10 nM) or HENECA (30 nM) facilitated GABA release by 32% and 21%, respectively. These effects were prevented by the A 2A antagonist, ZM 241385 (20 nM). A 2A receptors may activate adenylate cyclase and protein kinase A since CGS 21680 (10 nM) facilitation was partially prevented by 8-bromo-cAMP (1 mM), forskolin (10 μM) and HA-1004 (10 μM). Protein kinase C may also be recruited, since chelerythrine (6 μM) and phorbol-12,13-didecanoate (250 nM) attenuated CGS 21680 (10 nM) facilitation of [ 3H]GABA release. ω-Agatoxin-IVA (200 nM) occluded CGS 21680 facilitation suggesting the involvement of P-type calcium channels. Thus, the adenosine A 2A receptor system appears to be one of the first presynaptic neuromodulatory systems able to enhance the evoked release of GABA from hippocampal nerve terminals.
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