Maintaining the correct balance in neuronal activation is of paramount importance to normal brain function. Imbalances due to changes in excitation or inhibition can lead to a variety of disorders ranging from the clinically extreme (e.g. epilepsy) to the more subtle (e.g. anxiety). In the brain, the most common inhibitory synapses are regulated by GABAA (γ-aminobutyric acid type A) receptors, a role commensurate with their importance as therapeutic targets. Remarkably, we still know relatively little about GABAA receptor biogenesis. Receptors are constructed as pentameric ion channels, with α and β subunits being the minimal requirement, and the incorporation of a γ subunit being necessary for benzodiazepine modulation and synaptic targeting. Insights have been provided by the discovery of several specific assembly signals within different GABAA receptor subunits. Moreover, a number of recent studies on GABAA receptor mutations associated with epilepsy have further enhanced our understanding of GABAA receptor biogenesis, structure and function.
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October 2006
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Conference Article|
October 25 2006
The role of GABAA receptor biogenesis, structure and function in epilepsy
S. Mizielinska;
S. Mizielinska
1Neuroscience Institute, Ninewells Medical School, University of Dundee, Dundee DD1 9SY, U.K.
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S. Greenwood;
S. Greenwood
1Neuroscience Institute, Ninewells Medical School, University of Dundee, Dundee DD1 9SY, U.K.
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C.N. Connolly
C.N. Connolly
1
1Neuroscience Institute, Ninewells Medical School, University of Dundee, Dundee DD1 9SY, U.K.
1To whom correspondence should be addressed (email c.n.connolly@dundee.ac.uk).
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Publisher: Portland Press Ltd
Received:
July 06 2006
Online ISSN: 1470-8752
Print ISSN: 0300-5127
© 2006 The Biochemical Society
2006
Biochem Soc Trans (2006) 34 (5): 863–867.
Article history
Received:
July 06 2006
Citation
S. Mizielinska, S. Greenwood, C.N. Connolly; The role of GABAA receptor biogenesis, structure and function in epilepsy. Biochem Soc Trans 1 October 2006; 34 (5): 863–867. doi: https://doi.org/10.1042/BST0340863
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