Prolonged waking reduces human immunodeficiency virus glycoprotein 120- or tumor necrosis factor alpha-induced apoptosis in the cerebral cortex of rats

被引:5
作者
Montes-Rodríguez, CJ
Alavez, S
Elder, JH
Haro, R
Morán, J
Prospéro-García, O
机构
[1] Univ Nacl Autonoma Mexico, Inst Fisiol Celular, Dept Neurociencias, Lab BL 302, Mexico City 04510, DF, Mexico
[2] Univ Nacl Autonoma Mexico, Fac Med, Dept Fisiol, Grp Neurociencias, Mexico City 04510, DF, Mexico
[3] Scripps Res Inst, Dept Mol Biol, La Jolla, CA USA
关键词
apoptosis; cytokines; human immunodeficiency virus; neuroprotection; neurotrophic factors; total deprivation of sleep;
D O I
10.1016/j.neulet.2004.02.053
中图分类号
Q189 [神经科学];
学科分类号
071006 ;
摘要
The human immunodeficiency virus (HIV) induces neuronal death, presumably by apoptosis. This effect may be triggered by the glycoprotein 120 (HIVgp120) released by HIV when infecting a cell, and mediated by tumor necrosis factor alpha (TNFalpha), a pro-inflammatory cytokine. Both molecules, HIVgp120 and TNFalpha, increase sleep when administered acutely in the brain. On the other hand, sleep deprivation increases the levels of several growth factors. In this context, we challenged rats with HIVgp120 or TNFalpha simultaneously with sleep deprivation. Our results indicate that both HIVgp120 and TNFalpha increase neuronal death in the rat cerebral cortex, but not hippocampus, and that this effect is completely prevented by total deprivation of sleep. These results suggest that acute total deprivation of sleep protects against the HIVgp120 and TNFalpha deleterious effects. (C) 2004 Elsevier Ireland Ltd. All rights reserved.
引用
收藏
页码:133 / 136
页数:4
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