g-Amino Butyric Acid (GABA) is an inhibitory neurotransmitter. The abnormal increase in neuronal activity that is observed in epileptic seizures can be controlled in many cases by increasing the activity of the GABA-A receptors . GABA-A receptors are Chloride ion channels, and opening of the Chloride ion channels lowers the membrane potential, resulting in an increase in the time or activation required for crossing the threshold for activation of neuronal firing. Increase in GABA-ergic activity is the basis for the mechanism of action of several antiepileptic drugs . For example, Clobazam, barbiturates such as Phenobarbital, and benzodiazepines such as Diazepam are GABA receptor agonists, Tigabine inhibits re-uptake of GABA into the synaptic vescicles and increases the concentration of GABA in the synaptic cleft, and Vigabatrin inhibits GABA degradation by inhibition of the enzyme GABA transaminase (GABA-T) . The anti-epileptic drugs Valproate and Gabapentin are modulators of the enzyme glutamic acid decarboxylase (GAD) which catalyzes the conversion of glutamate to GABA. Some of these anti-epileptic drugs have multiple targets . For example, Valproate targets Sodium channels for modulating the membrane potential and T-type Calcium channels for modulating neurotransmitter release . And Gabapentine targets Calcium channels and increases intracellular concentration of GABA .