| First Author | Savitt JM | Year | 2005 |
| Journal | J Neurosci | Volume | 25 |
| Issue | 29 | Pages | 6721-8 |
| PubMed ID | 16033881 | Mgi Jnum | J:99848 |
| Mgi Id | MGI:3584064 | Doi | 10.1523/JNEUROSCI.0760-05.2005 |
| Citation | Savitt JM, et al. (2005) Bcl-x is required for proper development of the mouse substantia nigra. J Neurosci 25(29):6721-8 |
| abstractText | Recent findings have uncovered a role for the Bcl-x gene in the survival of dopaminergic neurons. The exact nature of this role has been difficult to examine because of the embryonic lethality of Bcl-x gene disruption in mouse models. Here we report the generation catecholaminergic cell-specific conditional Bcl-x gene knock-out mice using Cre-lox recombination technology. First we produced transgenic mice that express Cre recombinase from an exogenous rat tyrosine hydroxylase promoter (TH-Cre mice). These mice were crossed to Z/AP and Z/EG reporter mouse strains to verify catecholaminergic (TH-positive) cell-specific Cre expression. The TH-Cre mice then were mated to mice possessing the Bcl-x gene flanked by loxP sites, thereby producing offspring with Bcl-x deletion limited to catecholaminergic cells. The resulting mice are viable but have one-third fewer catecholaminergic neurons than do control animals. They demonstrate a deficiency in striatal dopamine and also tend to be smaller and have decreased brain mass when compared with controls. Surprisingly, surviving neurons were found that lacked Bcl-x immunoreactivity, thereby demonstrating that this gene is dispensable for the ongoing survival of a subpopulation of catecholaminergic cells. |
