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

✍ Scribed by Corinne Haller; Emilio Casanova; Matthias Müller; Claire-Marie Vacher; Rejan Vigot; Thierry Doll; Samuel Barbieri; Martin Gassmann; Bernhard Bettler

• Publisher: John Wiley and Sons
• Year: 2004
• Tongue: English
• Weight: 265 KB
• Volume: 40
• Category: Article
• ISSN: 1526-954X
• DOI: 10.1002/gene.20073

✦ Synopsis

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 lox511 sites. GABA(B(1)) (lox511/lox511) mice exhibit normal levels of GABA(B(1)) protein, are fertile, and do not display any behavioral phenotype. We crossed GABA(B(1)) (lox511/lox511) 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.