| First Author | Haller C | Year | 2004 |
| Journal | Genesis | Volume | 40 |
| Issue | 3 | Pages | 125-30 |
| PubMed ID | 15493018 | Mgi Jnum | J:94234 |
| Mgi Id | MGI:3511643 | Doi | 10.1002/gene.20073 |
| Citation | Haller C, et al. (2004) Floxed allele for conditional inactivation of the GABA(B(1)) gene. Genesis 40(3):125-30 |
| abstractText | 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. genesis 40:125-130, 2004. (c) 2004 Wiley-Liss, Inc. |
