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dc.contributor.author Khazipov R.
dc.date.accessioned 2018-09-19T22:23:51Z
dc.date.available 2018-09-19T22:23:51Z
dc.date.issued 2016
dc.identifier.uri https://dspace.kpfu.ru/xmlui/handle/net/145164
dc.description.abstract © 2016 Cold Spring Harbor Laboratory Press; all rights reserved. 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, maywork as a powerful synchronizing mechanism during epilepsy.
dc.title GABAergic synchronization in epilepsy
dc.type Article
dc.relation.ispartofseries-issue 2
dc.relation.ispartofseries-volume 6
dc.collection Публикации сотрудников КФУ
dc.source.id SCOPUS-2016-6-2-SID84956684756


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  • Публикации сотрудников КФУ Scopus [24551]
    Коллекция содержит публикации сотрудников Казанского федерального (до 2010 года Казанского государственного) университета, проиндексированные в БД Scopus, начиная с 1970г.

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