[Sodium valproate--current status of pharmacological research].
Valproic acid has a wider antiepileptic spectrum than any other antiepileptic drug (AED) in clinical use. Valproate administration causes many neurochemical and neurophysiological alterations, including increased GABA levels, modified GABA turnover and release, decreased gamma-hydroxybutyrate synthesis and release, increased serotonin and dopamine release, decreased aspartate levels, reduction of repetitive firing of neurons, and possibly a reduction in calcium (T) currents; however, none of these effects have consistently and unequivocally been linked to the antiepileptic action of valproate.
Chapman
A G
AG
Department of Neurology, Institute of Psychiatry, London, England.
D000818:Animals; D002118:Calcium / Q000378:metabolism; D004298:Dopamine / Q000378:metabolism; D006801:Humans; D007473:Ion Channels / Q000187:drug effects; D051381:Rats; D012701:Serotonin / Q000378:metabolism; D012978:Sodium Oxybate / Q000378:metabolism; D014635:Valproic Acid / Q000494:pharmacology*; D005680:gamma-Aminobutyric Acid / Q000378:metabolism
D007473:Ion Channels; D012701:Serotonin; D005680:gamma-Aminobutyric Acid; D014635:Valproic Acid; D012978:Sodium Oxybate; D002118:Calcium; D004298:Dopamine