Increased apoptosis in rat brain after rapid eye movement sleep loss

Biswas, Sudipta; Mishra, P. K.; Mallick, Birendra Nath

doi:10.1016/j.neuroscience.2006.06.026

Cited by 82 publications

(70 citation statements)

References 54 publications

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“…These cell stresses can ultimately progress to apoptosis. Whether neurodegeneration occurs following sleep deprivation remains controversial, with some studies reporting that sleep deprivation (both total and REM sleep) leads to the upregulation of apoptotic genes and increased cell death [194,202–204,277–279] and others reporting no evidence for degeneration by either morphological or expression data [248,280]. …”

Section: The Cellular Consequences Of Normal and Prolonged Wakefulmentioning

confidence: 99%

Sleep, Plasticity and the Pathophysiology of Neurodevelopmental Disorders: The Potential Roles of Protein Synthesis and Other Cellular Processes

et al. 2014

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Sleep is important for neural plasticity, and plasticity underlies sleep-dependent memory consolidation. It is widely appreciated that protein synthesis plays an essential role in neural plasticity. Studies of sleep-dependent memory and sleep-dependent plasticity have begun to examine alterations in these functions in populations with neurological and psychiatric disorders. Such an approach acknowledges that disordered sleep may have functional consequences during wakefulness. Although neurodevelopmental disorders are not considered to be sleep disorders per se, recent data has revealed that sleep abnormalities are among the most prevalent and common symptoms and may contribute to the progression of these disorders. The main goal of this review is to highlight the role of disordered sleep in the pathology of neurodevelopmental disorders and to examine some potential mechanisms by which sleep-dependent plasticity may be altered. We will also briefly attempt to extend the same logic to the other end of the developmental spectrum and describe a potential role of disordered sleep in the pathology of neurodegenerative diseases. We conclude by discussing ongoing studies that might provide a more integrative approach to the study of sleep, plasticity, and neurodevelopmental disorders.

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Section: The Cellular Consequences Of Normal and Prolonged Wakefulmentioning

confidence: 99%

Sleep, Plasticity and the Pathophysiology of Neurodevelopmental Disorders: The Potential Roles of Protein Synthesis and Other Cellular Processes

et al. 2014

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“…Dendrin was originally identified in sleep-deprived rats (18), a condition that induces neuronal apoptosis (19). In normal podocytes, dendrin is a constituent of the glomerular slit diaphragm, where it binds to nephrin and CD2-associated protein (CD2AP) (17).…”

Section: Yapmentioning

confidence: 99%

Yes-associated Protein (YAP) Promotes Cell Survival by Inhibiting Proapoptotic Dendrin Signaling

Campbell

Wong

Gupta

et al. 2013

Journal of Biological Chemistry

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“…way for brain recovery during sleep could be through neuroglobin synthesis; these proteins could help to improve neuronal survival by ROS degradation, oxygen transport facilitation and NAD+ regeneration under hypoxia conditions. Interestingly, 3 days of sleep recovery after REMSD are sufficient to counteract these cellular changes (Biswas et al, 2006;Majumdar & Mallick, 2005). These results suggest that sleep could prevent neuronal damage through the maintenance of cell integrity and neuronal survival by preservation of cytoskeleton proteins (Biswas et al, 2006), regulation of anti-and pro-apoptotic protein expression (Biswas et al, 2006;Montes-Rodriguez et al, 2009) or through the expression of genes involved in the maintenance of different cellular processes; such as cholesterol and protein synthesis, synaptic vesicle formation, antioxidant enzymes synthesis, etc.…”

Section: Brain Restoration As a Sleep Functionmentioning

confidence: 93%

“…Furthermore, 6 days of REMSD affect both size and shape of neurons present in locus ceruleus (LC) and PPT/LDT nucleus, regions involved in REM sleep regulation (Majumdar & Mallick, 2005), there is also an increase in neuronal expression of pro-apoptotic genes (i.e. Bax) and a decrease in actin and tubulin levels (Biswas et al, 2006). Fig.…”

Section: Brain Restoration As a Sleep Functionmentioning

confidence: 99%