A deficit of functional GABA(A) receptors in neurons of beta 3 subunit knockout mice.
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.
Krasowski
M D
MD
Committee on Neurobiology, University of Chicago, IL 60637, USA.
Rick
C E
CE
Harrison
N L
NL
Firestone
L L
LL
Homanics
G E
GE
D000818:Animals; D002478:Cells, Cultured; D004357:Drug Synergism; D005727:Ganglia, Spinal / Q000187:drug effects / Q000378:metabolism / Q000502:physiology; D006624:Hippocampus / Q000187:drug effects / Q000378:metabolism / Q000502:physiology; D051379:Mice; D018345:Mice, Knockout / Q000502:physiology*; D009474:Neurons / Q000166:cytology / Q000378:metabolism* / Q000502:physiology; D018408:Patch-Clamp Techniques; D011963:Receptors, GABA-A / Q000172:deficiency* / Q000187:drug effects / Q000235:genetics*
D011963:Receptors, GABA-A