The involvement of taurine in the action mechanism of sodium valproate (VPA) in the treatment of epilepsy

Abstract

Several lines of evidence have shown that sodium valproate (VPA) mechanism of action in the therapy of epilepsy is based on the phenomena of its interaction with neurotransmitters (GABA), receptor sites and ion channels (1). However, there is no conclusive evidence to show the extent of VPA interactions with other neurotransmitters in the brain. Based on this fact, taurine (an amino acid 'neurotransmitter') found distributed in the brain the visual system may probably be involved in the drug action mechanism of VPA. The application of taurine in experimental and human epilepsy started over thirty years ago (2,3) and it has been known to possess some mild anticonvulsant activity in both humans and experimental animal models (4). This review, therefore, will attempt to draw together all the available information on the involvement of taurine in epilepsy and its possible association with the action mechanism of VPA in suppressing epileptic seizures. Structural and physiological distribution of taurine in the brain will be discussed. Its association with the phenomena of VPA action in epilepsy will be cited. Its neurotransmitter candidacy, involvement in ocular pathology, receptor sites and modulatory activity will be dealt with in relation to valproate action in the therapy of epilepsy.