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A deficit of functional GABA(A) receptors in neurons of beta 3 subunit knockout mice
Journal article   Open access   Peer reviewed

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

Matthew D Krasowski, Caroline E Rick, Neil L Harrison, Leonard L Firestone and Gregg E Homanics
Neuroscience letters, Vol.240(2), pp.81-84
01/09/1998
DOI: 10.1016/s0304-3940(97)00929-4
PMID: 9486477
url
https://www.ncbi.nlm.nih.gov/pmc/articles/2846962View
Open Access

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.
Cells, Cultured Ganglia, Spinal - physiology Neurons - cytology Hippocampus - drug effects Receptors, GABA-A - deficiency Drug Synergism Hippocampus - metabolism Patch-Clamp Techniques Animals Receptors, GABA-A - genetics Neurons - physiology Receptors, GABA-A - drug effects Mice Neurons - metabolism Mice, Knockout - physiology Ganglia, Spinal - drug effects Hippocampus - physiology Ganglia, Spinal - metabolism

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