Role of caspase-3 in ethanol-induced developmental neurodegeneration

Chainllie Young, Kevin A. Roth, Barbara J. Klocke, Tim West, David M. Holtzman, Joann Labruyere, Yue Qin Qin, Krikor Dikranian, John W. Olney

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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.

Original languageEnglish
Pages (from-to)608-614
Number of pages7
JournalNeurobiology of Disease
Issue number2
StatePublished - Nov 1 2005


  • Alcohol
  • Apoptosis
  • Caspase-3 knockout
  • Development

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    Young, C., Roth, K. A., Klocke, B. J., West, T., Holtzman, D. M., Labruyere, J., Qin, Y. Q., Dikranian, K., & Olney, J. W. (2005). Role of caspase-3 in ethanol-induced developmental neurodegeneration. Neurobiology of Disease, 20(2), 608-614.