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Trends Neurosci. 2011 Feb;34(2):101-12. doi: 10.1016/j.tins.2010.10.005. Epub 2010 Dec 9.

GABA A,slow: causes and consequences.

Author information

1
MRC Anatomical Neuropharmacology Unit, Mansfield Road, Oxford OX1 3TH, UK. marco.capogna@pharm.ox.ac.uk

Abstract

GABA(A) receptors in the CNS mediate both fast synaptic and tonic inhibition. Over the past decade a phasic current with features intermediate between fast synaptic and tonic inhibition, termed GABA(A,slow), has received increasing attention. This has coincided with an ever-growing appreciation for GABAergic cell type diversity. Compared with classical fast synaptic inhibition, GABA(A,slow) is slower by an order of magnitude. In this review, we summarize recent studies that have enhanced our understanding of GABA(A,slow). These include the discovery of specialized interneuron types from which this current originates, the factors that could underlie its characteristically slow kinetics, its contribution to specific aspects of integrative function and network oscillations, and its potential usefulness as a novel drug target for modulating inhibitory synaptic transmission in the CNS.

PMID:
21145601
DOI:
10.1016/j.tins.2010.10.005
[Indexed for MEDLINE]

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