1The extracellular glutamate content and Ca2+ level in vivo in rat hippocampus were measured by brain microdialysis following administration of two depolarizing agents (veratridine, KCl) and quinolinic acid (Quin). 2 The two depolarizing agents increased the extracellular glutamate level (to between 280 and 320% basal) and decreased the extracellular Ca2" content (to 48% of basal). However, Quin did not change the glutamate level but decreased the Ca2+ content. 3 The effects of Ca2+ antagonists on the changes of glutamate and Ca2+ level were evaluated in this experimental model. At a dose of 0.5 mgkg-1, i.v., nimodipine (L-type channel blocker) did not produce significant changes in the stimulated-glutamate release. A statistically significant inhibition of Ca2 + influx was observed at a dose of 0.05 mg kg'-. In contrast, in those animals receiving the N-type Ca2 + antagonist, daurisoline (0.1, 1 or 5 mg kg ',i.v.), a potent attenuation of both glutamate release and Ca2 + influx was found. 4 We propose that the pharmacological properties of Ca2 + influx and of neurotransmitter release differ and that nimodipine-sensitive L-type channels may not be very common in nerve terminals but are localized in cell soma. Daurisoline-sensitive N-type channels in nerve terminals have a much greater influence on excitatory amino acid release.
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