Figure 2.

Diverse molecular targets for antiseizure drugs (ASDs) at inhibitory γ-aminobutyric acid (GABA)ergic synapses. Seizure protection can be conferred by effects on synaptic or extrasynaptic GABA_A receptors or on GABA transaminase (GABA-T) or GABA transporter 1 (GAT1). Furthermore, some ASDs (e.g., valproate) have been shown to increase the activity of the GABA-synthesizing enzyme glutamic acid decarboxylase (GAD), thereby increasing GABA turnover. Astrocytes contain elements, including GABA transporters, which influence the dynamics of GABA, thereby affecting the excitability of the postsynaptic neuron.