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Neurobiol Dis ; 18(3): 582-90, 2005 Apr.
Artigo em Inglês | MEDLINE | ID: mdl-15755684

RESUMO

Pilocarpine-induced status epilepticus (PCSE) is a widely used model to study neurodegeneration in limbic structures after prolonged epileptic seizures. However, mechanisms mediating neuronal cell death in this model require further characterization. Examining the expression time course and spatial distribution of activated caspase-3, we sought to determine the role of apoptosis in PCSE-mediated neuronal cell death. Expression of activated caspase-3, predominantly located in neurons, was detected 24 h (amygdala; piriform and temporal cortex) and 7 days (hippocampus; amygdala; piriform, temporal and parietal cortex; thalamus) after PCSE with strongest induction being observed in the amygdala, the piriform cortex, and the hippocampus. Further analysis revealed TUNEL positivity (24 h and 7 days after SE) and a significant, progressive neuronal cell loss in all brain regions displaying caspase-3 activation. Corresponding to high levels of activated caspase-3 expression, neuronal cell loss was most pronounced in the amygdala, piriform cortex, and dorsal CA-1 hippocampus. These results demonstrate that apoptosis contributes significantly to PCSE-induced neuronal cell death.


Assuntos
Caspases/biossíntese , Regulação Enzimológica da Expressão Gênica/fisiologia , Neurônios/enzimologia , Convulsões/enzimologia , Estado Epiléptico/enzimologia , Animais , Caspase 3 , Caspases/metabolismo , Morte Celular/fisiologia , Ativação Enzimática/genética , Masculino , Neurônios/química , Ratos , Ratos Sprague-Dawley , Fatores de Tempo
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