GABAergic Synchronization in Epilepsy
Author(s) -
Roustem Khazipov
Publication year - 2016
Publication title -
cold spring harbor perspectives in medicine
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 3.853
H-Index - 105
eISSN - 2472-5412
pISSN - 2157-1422
DOI - 10.1101/cshperspect.a022764
Subject(s) - gabaergic , neuroscience , glutamatergic , epilepsy , inhibitory postsynaptic potential , gamma aminobutyric acid , excitatory postsynaptic potential , glutamate receptor , biology , medicine , receptor
γ-Aminobutyric acid (GABA) is the main inhibitory neurotransmitter in the cerebral cortex. GABAergic inhibition enables synchronization of activity in cortical networks, and contributes to generation of variety of brain activity patterns. In relation to epilepsy, GABAergic inhibition has been traditionally viewed as the main mechanism counterbalancing glutamatergic excitation and preventing hypersynchronous neuronal discharges. Indeed, deficits in GABAergic functions most commonly result in a hyperexcitable epileptic state, and many of the currently used antiepileptic drugs act through enhancement of GABAergic functions. However, a number of observations show that some epileptiform activity patterns involve synchronization by GABAergic mechanisms. These include two main categories that will be reviewed here: (1) synchronization of epileptiform oscillations based on GABAergic inhibition, and (2) epileptiform events driven by depolarizing and excitatory GABA. The conclusion is reached that GABAergic control of spike timing, either through inhibition or excitation under certain conditions, may work as a powerful synchronizing mechanism during epilepsy.
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