PMID: 9486477Mar 5, 1998

A deficit of functional GABA(A) receptors in neurons of beta 3 subunit knockout mice

Neuroscience Letters
M D KrasowskiG E Homanics

Abstract

Mice whose gamma-aminobutyric acid type A (GABA(A)) beta3 subunit gene is inactivated ('beta3 knockout mice') have been previously shown to have epilepsy, hypersensitive behavior, cleft palate, and a high incidence of neonatal mortality. In this study, we analyze whole-cell responses to GABA in neurons from beta3+/+, beta3+/- and beta3-/- mice. We demonstrate markedly decreased responses to GABA in both hippocampal and dorsal root ganglion neurons isolated from beta3-/- mice without major differences in the GABA concentration-response curves. We also utilize the subunit selective pharmacology of Zn2+ and the anticonvulsant drug loreclezole to help infer the presence of beta2 and gamma subunits in the GABA(A) receptors remaining in neurons from beta3-/- mice.

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Aug 1, 1991·British Journal of Pharmacology·T G SmartR L Huganir
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Jan 1, 1994·Annual Review of Neuroscience·R L Macdonald, R W Olsen
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Related Concepts

BHLHE22 wt Allele
Anticonvulsants
Epilepsy
Loreclezole
Neurons
Entire Spinal Nerve Ganglion
Voltage-Clamp Techniques
GABA-A Receptor gamma Subunit
Mice, Knockout
NEUROD1 wt Allele

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