Sleep deprivation does not affect indices of necrosis or apoptosis in rat brain

Sleep deprivation does not affect indices of necrosis or apoptosis in rat brain

Autor Hipólide, Débora Cristina Autor UNIFESP Google Scholar
D'Almeida, Vania Autor UNIFESP Google Scholar
Raymond, Roger Google Scholar
Tufik, Sergio Autor UNIFESP Google Scholar
Nobrega, J. N. Google Scholar
Instituição Ctr Addict & Mental Hlth
Universidade Federal de São Paulo (UNIFESP)
Resumo Recent indications of oxidative stress in hypothalamus of sleep deprived rats prompted us to address the possibility that sleep deprivation may induce pathological cell loss changes in brain. Indices of necrosis and apoptosis were quantified after 96 h of sleep deprivation induced by the classical platform technique in rats. Binding of the peripheral-type benzodiazepine ligand [H-3] PK 11195 to reactive astrocytes, a reliable and sensitive index of necrotic changes, was not altered in any of 14 brain regions examined. Likewise, no changes were found in mRNA levels of the apoptosis-related genes bcl-2 and bax in any of 24 brain regions examined. This was corroborated by quantitative TUNEL analyses in hypothalamus, amygdala, and cortex, which also revealed no effects in sleep deprived animals. These results are consistent with other recent evidence that sleep deprivation does not induce necrotic or apoptotic cell loss in brain. This suggests that recent findings of oxidative stress in sleep deprived brains do not result in cell loss. the possibility that sleep deprivation may result in functional deficits, or that structural changes may emerge after repeated episodes of sleep deprivation, remains to be addressed.
Palavra-chave apoptosis
autoradiography
bax
bcl-2
gliosis
in situ hybridization
neuropathology
omega(3) receptors
[H-3] PK 11195
TUNEL
Idioma Inglês
Data de publicação 2002-02-01
Publicado em International Journal of Neuroscience. Abingdon: Taylor & Francis Ltd, v. 112, n. 2, p. 155-166, 2002.
ISSN 0020-7454 (Sherpa/Romeo, fator de impacto)
Publicador Taylor & Francis Ltd
Extensão 155-166
Fonte http://dx.doi.org/10.1080/00207450212022
Direito de acesso Acesso restrito
Tipo Artigo
Web of Science WOS:000175942300004
Endereço permanente http://repositorio.unifesp.br/handle/11600/26752

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