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PMID: 1664056 Published · ppublish English Journal Article Research Support, Non-U.S. Gov't Research Support, U.S. Gov't, P.H.S. Review

Electrophysiology of GABA-mediated synaptic transmission and possible roles in epilepsy.

Neurochemical research ·Vol. 16 ·No. 3 ·1991-03-00 ·Pages 251-62

Tasker JG, Dudek FE

Abstract

Epileptogenic conditions come about from a disequilibrium between excitatory and inhibitory mechanisms, creating a state of neuronal hypersynchrony. From experimental studies in animal models of epilepsy it appears that several mechanisms, alone or in combination, could be responsible for this imbalance. An alteration of GABA-mediated inhibition has long been considered to be one of the most likely candidates. We review recent data on the synaptic physiology of GABA-mediated inhibition, with emphasis on GABAA and GABAB receptors and their conductances. We describe the integrative role of GABAergic local-circuit neurons in the normal control of recurrent excitation. We then discuss possible alterations in GABAA-mediated inhibition in two chronic animal models of epilepsy, the kindled rat and the kainate-treated rat. Finally, we review studies on GABA inhibition in human epileptic cortex resected for the treatment of intractable epilepsy.

MeSH Terms
Animals Electrophysiology Epilepsy/physiopathology Humans Receptors, GABA-A/physiology Synapses/physiology Synaptic Transmission/physiology gamma-Aminobutyric Acid/physiology
Chemicals
Receptors, GABA-A gamma-Aminobutyric Acid
Authors & Affiliations
2 authors, click to expand affiliations / ORCID
Tasker J G
Mental Retardation Research Center, UCLA School of Medicine 90024.
Dudek F E
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Article Info
Journal
Neurochemical research
Abbr.
Neurochem Res
ISSN
0364-3190
DOI
10.1007/BF00966088
Published
1991-03-00
Pages
251-62
Language
English
Region
United States
NLM ID
7613461
Subset
IM
Grants
NINDS NIH HHS · NS16683 · United States
External Links
PubMed source DOI: 10.1007/BF00966088 View journal details
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