Role of caspase-3 in ethanol-induced developmental neurodegeneration.
Neurobiol Dis
; 20(2): 608-14, 2005 Nov.
Article
en En
| MEDLINE
| ID: mdl-15927478
ABSTRACT
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.
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Bases de datos:
MEDLINE
Asunto principal:
Encéfalo
/
Apoptosis
/
Caspasas
/
Trastornos del Sistema Nervioso Inducidos por Alcohol
/
Etanol
/
Degeneración Nerviosa
Tipo de estudio:
Prognostic_studies
Límite:
Animals
Idioma:
En
Revista:
Neurobiol Dis
Asunto de la revista:
NEUROLOGIA
Año:
2005
Tipo del documento:
Article
País de afiliación:
Estados Unidos