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Presynaptic Modulation of Glutamate Release Targets Different Calcium Channels in Rat Cerebrocortical Nerve Terminals

We have studied which type/s of Ca2+ ‐channel/s support glutamate exocytosis and its modulation by presynaptic receptors in cerebrocortical nerve terminals. Depolarization of nerve terminals with 30 mM KCI induced a Ca2+ ‐dependent release of 3.64 ± 0.25 nmol/mg of protein. The addition of either 2 μM ω‐conotoxin‐GVIA or 200 nM ω‐agatoxin‐IVA reduced the KCI‐evoked release by 47.7 ± 3.5% and 70.4 ± 8.9% respectively, and by 85.7 ± 4.1% when both toxins were co‐applied. The activation of adenosine A1 receptors with N6‐cyclohexyladenosine or the activation of rnetabotropìc glutamate receptors with L(+)‐2‐amino‐4‐phosphonobutyrate inhibited the KCI‐evoked release by 41.0 ± 5.9 and 54.3 ± 10% respectively. The extent of these inhibitions was not altered by the prior addition of 2 μM ω‐conotoxin‐GVIA but they were significantly enhanced when ω‐agatoxin‐IVA was added together with the adenosine A1 receptor agonist or the metabotropic glutamate receptor agonist, suggesting that ω‐conotoxin‐GVIA‐sensitive and not ω‐agatoxin‐IVA‐sensitive Ca2+‐channels are ínvolved in the action of these inhibitory receptors. By contrast, the facilitation of glutamate release that follows the activation of the protein kinase C, either with phorbol esters or with the stimulation of phospholipase C‐linked metabotropic receptors, was expressed by both ω‐conotoxin‐GVIA‐sensitive and ω‐agatoxin‐sensitive Ca2+‐channels. It is concluded that different Ca2+‐channels support the modulation of glutamate release by presynaptic receptors.