The neuroprotective drug vinpocetine prevents veratridine-induced [Na+]i and [Ca2+]i rise in synaptosomes

THE effect of the neuroprotective drug, vinpocetine on the veratridine-evoked [Na+](i) and [Ca2+](i) rise in isolated nerve terminals was studied. Vinpocetine, in a pharmacologically relevant concentration range (0.4-10 mu M)(i) reduced the increase of [Na+](i) induced by veratridine (100 mu M). The effect of the drug was concentration-dependent with 10 mu M vinpocetine completely preventing the increase of [Na+](i). The [Ca2+](i) rise in response to veratridine was also prevented by vinpocetine. In addition, the [Ca2+](i) signal induced by depolarization with 20 mM K+ was reduced by vinpocetine (1-20 mu M) This effect was not influenced by preincubation with 1 mu M TTX and was also observed when Na+ was replaced by N-methyl glucamine in the medium. It is concluded that vinpocetine is capable of inhibiting voltage-dependent Na+ and Ca2+ channels, respectively, and these effects might contribute to the neuroprotection exerted by the drug. (C) 1998 Rapid Science Ltd.