The antiepileptic effect of Sodium valproate (VPA) was serendipotously discovered in 1963, but only later were its action mechanisms understood. VPA inhibits GABA transaminase thus enhancing the cerebral levels of the inhibitory neurotransmitter Gamma-aminobutyric acid (GABA), but this effect is obtained only at concentrations higher than those clinically effective. VPA reduces the sodium membrane conductance thus depressing the generation and transmission of action potential signals responsible for neurotransmitter release from presynaptic terminations. This effect involves also the non inactivating component of sodium current underlying bursting discharge of neurons responsible for cortical synchronization which is therefore reduced by VPA. Finally VPA slightly reduces the low threshold calcium current of thalamic neurons responsible for spike-wave generation. The possible correlation between the multiplicity of the action mechanisms and the broad spectrum of clinical efficacy of VPA is discussed.
|Translated title of the contribution||Biological basis of clinical effect of sodium valproate|
|Number of pages||6|
|Journal||Bollettino - Lega Italiana contro l'Epilessia|
|Issue number||95-96 SUPPL. 1|
|Publication status||Published - 1996|
ASJC Scopus subject areas
- Clinical Neurology