Figure 8

Figure 8

(A) Docking study of embelin with respect to diazepam and the GABA_A receptor. (B) Proposed mechanism of action of embelin at the GABA_A receptor to reverse PTZ induced seizures. 8B1—During a seizure, a prolonged opening of the voltage-gated Na⁺ channel causes an influx of sodium ions which leads to depolarization and repetitive neuronal firing. The opening of Ca2⁺ channels increases the influx of positive calcium ions causing prolonged spikes and T current waves. As there is no affinity for the GABAA receptor, the decreased Cl⁻ influx causes epileptic excitation inside the neuron cell. 8B2—EMB shows higher affinity for GABA_A receptor binding; it facilitates GABA mediated Cl⁻ channel opening with cell hyperpolarization and reduced seizure frequency, prolonged inactivation of the voltage-gated neuronal Na+ channel, prevented intracellular Na+ accumulation, reduced Ca2⁺ influx, and inhibited glutamate.