The role of Ca 2 + in the protoveratrine - induced release of y - aminobutyrate from rat brain slices

1. Protoveratrine A increased the release of y-aminoPHlbutyrate from small slices of rat cerebral cortex. This effect increased with increasing protoveratrine concentration, reaching a maximum at 100,M. 2. Removal of Ca2+ from the superfusing medium did not change the increase in release due to 10,uM-protoveratrine; however, the Ca2+ antagonists, compound D-600, La3+, Mn2+, Mg2+ and also high Ca2+ concentration inhibited the effect of the alkaloid, as did procaine. 3. Protoveratrine A increased the uptake of 22Na+ into the slices with a similar dose-response curve to that found for y-aminobutyrate release. For the most part, the substances that inhibited protoveratrine-stimulated y-aminobutyrate release also inhibited 22Na+ u-ptake, although the correlation was not perfect. 4. Although extracellular Ca2+ is not required for protoveratrine-induced y-aminobutyrate release, an increase in Nat influx that is susceptible to inhibition by some Ca2+ antagonists does appear to be associated with this phenomenon. However, the possibility remains that changes in the free intracellular Ca2+ concentration may be important for transmitter release induced by depolarizing veratrum alkaloids.