| First Author | Young C | Year | 2005 |
| Journal | Neurobiol Dis | Volume | 20 |
| Issue | 2 | Pages | 608-14 |
| PubMed ID | 15927478 | Mgi Jnum | J:124443 |
| Mgi Id | MGI:3721718 | Doi | 10.1016/j.nbd.2005.04.014 |
| Citation | Young C, et al. (2005) Role of caspase-3 in ethanol-induced developmental neurodegeneration. Neurobiol Dis 20(2):608-14 |
| abstractText | Acute, transient exposure to ethanol causes a widespread pattern of caspase-3 activation and neuroapoptosis in the developing rodent brain. To determine whether caspase-3 activation is an essential step in ethanol-induced developmental neuroapoptosis, we treated homozygous caspase-3 knockout mice or wild-type mice on postnatal day 7 with an apoptosis-inducing dose of ethanol and examined the brains at appropriate survival times for evidence of apoptotic neurodegeneration. In caspase-3 knockout mice, the cell death process evolved more slowly than in wild-type mice, and morphological changes observed were not those typically associated with apoptosis. However, neuronal cell counts performed 2 weeks post-treatment revealed that the extent of neuron loss was similar in wild-type and caspase-3-deficient mice. We conclude that absence of functional caspase-3 alters the time course and morphological characteristics of the neurodegenerative process but does not prevent ethanol-induced neuron death. |
