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

Neurosci Lett. 1998 Jan 9;240(2):81-4. doi: 10.1016/s0304-3940(97)00929-4.


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.

MeSH terms

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


  • Receptors, GABA-A