The role of Ca2+ in the protoveratrine-induced release of γ-aminobutyrate from rat brain slices

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Abstract
Protoveratrine A increased the release of .gamma.-amino[3H]butyrate from small slices of rat cerebral cortex. This effect increased with increasing protoveratrine concentration, reaching a maximum at 100 .mu.M. Removal of Ca2+ from the superfusing medium did not change the increase in release due to 10 .mu.M-protoveratrine; the Ca2+ antagonists, compound D-600 [methoxy verapamil], La3+, Mn2+ and Mg2+, procaine and high Ca2+ concentration inhibited the effect of the alkaloid. Protoveratrine A increased the uptake of 22Na+ into the slices with a dose-response curve similar to .gamma.-aminobutyrate release. The substances inhibiting protoveratrine-stimulated .gamma.-aminobutyrate release usually inhibited 22Na+ uptake, although the correlation was not perfect. Although extracellular Ca2+ was not required for protoveratrine-induced .gamma.-aminobutyrate release, an increase in Na+ influx that is susceptible to inhibition by some Ca2+ antagonists did appear associated. Changes in the free intracellular Ca2+ concentration may be important for transmitter release induced by depolarizing veratrum alkaloids.

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