• Chainllie Young, Kevin A Roth, Barbara J Klocke, Tim West, David M Holtzman, Joann Labruyere, Yue-Qin Qin, Krikor Dikranian, and John W Olney.
• Department of Psychiatry, Campus box 8134, Washington University School of Medicine, 660 South Euclid, St. Louis, MO 63110, USA.
• Neurobiol. Dis. 2005 Nov 1; 20 (2): 608-14.

AbstractAcute, 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.

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