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. 2019 Oct 25;10:1249. doi: 10.3389/fphar.2019.01249

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Copyright © 2019 Kundap, Choo, Kumari, Ahmed, Othman and Shaikh

This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) and the copyright owner(s) are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.

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(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.