Abstract
Temporal lobe epilepsy (TLE), as a most common type of ungovernable epilepsy is characterized by reduced inhibitory network activity. GABAergic neurotransmission undergoes perturbation and depression in its inhibitory function such as, recapitulation; changes in expression of KCC1 and NKCC2 co-transporters which regulate Cl- homeostasis, alteration in expression and arrangement of subunits of GABA receptors specially GABAA (Cl- channel), sprouting and reorganization of GABAergic neurons and many alterations that we don’t account for in this review. All of these changes lead in reduction of GABAergic inhibitory effects, so it can induce epileptic activity in neuronal networks. Understanding the mechanisms of such reorganization and alterations can help us to develop more potent novel therapeutic materials for TLE patients.
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