Floxed allele for conditional inactivation of the GABABB(1) gene

被引:45
作者
Haller, C
Casanova, E
Müller, M
Vacher, CM
Vigot, R
Doll, T
Barbieri, S
Gassmann, M
Bettler, B
机构
[1] Univ Basel, Inst Physiol, Pharmzentrum, Dept Clin Biol Sci, CH-4056 Basel, Switzerland
[2] Novartis Pharma AG, Novartis Inst Biomed Res, Basel, Switzerland
关键词
GABA(B); gamma-aminobutyric acid; baclofen; metabotropic; Cre-recombinase;
D O I
10.1002/gene.20073
中图分类号
Q [生物科学];
学科分类号
07 ; 0710 ; 09 ;
摘要
GABA(B) receptors are the G-protein-coupled receptors for the neurotransmitter GABA. GABA(B) receptors are broadly expressed in the nervous system. Their complete absence in mice causes premature lethality or-when mice are viable- epilepsy, impaired memory, hyperalgesia, hypothermia, and hyperactivity. A spatially and temporally restricted loss of GABA(B) function would allow addressing how the absence of GABA(B) receptors leads to these diverse phenotypes. To permit a conditional gene inactivation, we flanked critical exons of the GABA(B(1)) gene with Iox511 sites. GABA(B(1))(Iox511/Iox511) mice exhibit normal levels of GABA(B(1)) protein, are fertile, and do not display any behavioral phenotype. We crossed GABA(B(1))(Iox511/Iox511) with Cre-deleter mice to produce mice with an unrestricted GABA(B) receptor elimination. These GABA(B(1))(-/-) mice no longer synthesize GABA(B(1)) protein and exhibit the expected behavioral abnormalities. The conditional GABA(B(1)) allele described here is therefore suitable for generating mice with a site and time-specific loss of GABA(B) function. genesis 40: 125-130, 2004. (C) 2004 Wiley-Liss, Inc.
引用
收藏
页码:125 / 130
页数:6
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