β3亚基基因敲除小鼠神经元中功能性γ-氨基丁酸A（GABA(A)）受体缺乏。
A deficit of functional GABA(A) receptors in neurons of beta 3 subunit knockout mice.
作者信息
Krasowski M D, Rick C E, Harrison N L, Firestone L L, Homanics G E
机构信息
Committee on Neurobiology, University of Chicago, IL 60637, USA.
出版信息
Neurosci Lett. 1998 Jan 9;240(2):81-4. doi: 10.1016/s0304-3940(97)00929-4.
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.
摘要
先前已表明，γ-氨基丁酸A型（GABA(A)）β3亚基基因失活的小鼠（“β3基因敲除小鼠”）患有癫痫、行为过敏、腭裂且新生儿死亡率很高。在本研究中，我们分析了来自β3+/+、β3+/-和β3-/-小鼠神经元对GABA的全细胞反应。我们证明，从β3-/-小鼠分离的海马体和背根神经节神经元对GABA的反应均显著降低，而GABA浓度-反应曲线无重大差异。我们还利用Zn2+的亚基选择性药理学以及抗惊厥药物氯雷唑来帮助推断β3-/-小鼠神经元中剩余的GABA(A)受体中β2和γ亚基的存在情况。
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