The mechanisms of therapeutic actions Valproic Acid (VPA) are not well understood. It may act by increasing gamma-aminobutyric acid levels in the brain or by altering the properties of voltage dependent sodium channels.
VPA, or its sodium salt, dissociates to the valproate ion in the gastrointestinal tract or in the blood and then binds to and inhibits GABA transaminase. Therefore, the drug’s anticonvulsant activity may be, at least partly, related to increased brain concentrations of gamma-aminobutyric acid (GABA), an inhibitory neurotransmitter in the CNS, by inhibiting enzymes that catabolize GABA or block the reuptake of GABA into glia and nerve endings. Both these actions increase concentrations of GABA in the brain. A second major hypothesis for VPA’s action is that it enhances neuronal responsiveness to GABA. All these actions result in potentiation of the synaptic actions of GABA.
Other actions that may contribute to VPA’s therapeutic effects include a decrease in dopamine turnover, a decrease in the activity of the NMDA-glutamate receptors and also a decrease in the concentration of somatostatin in the CSF.
VPA may also work by suppressing repetitive neuronal firing through inhibition of voltage-sensitive sodium channels, thereby creating a direct membrane-stabilizing effect. Some studies suggest that VPA may also affect potassium channels.
VPA is also likely to produce its anti-manic effects through its GABAergic effects, where VPA leads to a rise in cerebral and cerebellar levels of GABA, possibly by inhibiting GABA degradative enzymes, such as GABA transaminase and succinate-semialdehyde dehydrogenase, and also by inhibiting the re-uptake of GABA by neuronal cells.
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