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

Neuroreport. 1998 Jun 1;9(8):1849-53. doi: 10.1097/00001756-199806010-00034.

Abstract

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 microM)i reduced the increase of [Na+]i induced by veratridine (100 microM). The effect of the drug was concentration-dependent with 10 microM 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 microM). This effect was not influenced by preincubation with 1 microM 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.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Animals
  • Calcium / metabolism*
  • Guinea Pigs
  • In Vitro Techniques
  • Membrane Potentials / drug effects
  • Neuroprotective Agents / pharmacology*
  • Sodium / metabolism*
  • Synaptosomes / drug effects*
  • Synaptosomes / metabolism
  • Veratridine / pharmacology*
  • Vinca Alkaloids / pharmacology*

Substances

  • Neuroprotective Agents
  • Vinca Alkaloids
  • vinpocetine
  • Veratridine
  • Sodium
  • Calcium