Sleep deprivation induced by the modified multiple platform technique: quantification of sleep loss and recovery

Machado, Ricardo Borges; Hipólide, Débora Cristina; Benedito‐Silva, Ana Amélia; Tufik, Sérgio

doi:10.1016/j.brainres.2004.01.019

Cited by 346 publications

(240 citation statements)

References 31 publications

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“…A rebound in cell proliferation and adult neurogenesis was eventually observed after prolonged sleep deprivation, but this did not emerge until considerably after the time when normal sleep patterns reestablish (23). In contrast to the glucocorticoidmediated suppression of cell proliferation, the increase in cell proliferation and neurogenesis observed 1 wk later persisted despite normalized CORT levels.…”

Section: Discussionmentioning

confidence: 95%

“…Six hours after prolonged sleep deprivation, a time characterized by maximal REM rebound (22), cell proliferation remained inhibited. But 1 wk later, when animals have resumed normal sleep patterns (21,23), the production of new cells exceeds that of controls. This overshoot in cell proliferation does not seem linked to glucocorticoids, because clamping CORT levels throughout the sleep deprivation and recovery period does not eliminate this effect.…”

Section: Discussionmentioning

confidence: 98%

See 1 more Smart Citation

Sleep deprivation inhibits adult neurogenesis in the hippocampus by elevating glucocorticoids

Mirescu

Peters²,

Noiman³

et al. 2006

Proc. Natl. Acad. Sci. U.S.A.

204

137

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Prolonged sleep deprivation is stressful and has been associated with adverse consequences for health and cognitive performance. Here, we show that sleep deprivation inhibits adult neurogenesis at a time when circulating levels of corticosterone are elevated. Moreover, clamping levels of this hormone prevents the sleep deprivation-induced reduction of cell proliferation. The recovery of normal levels of adult neurogenesis after chronic sleep deprivation occurs over a 2-wk period and involves a temporary increase in new neuron formation. This compensatory increase is dissociated from glucocorticoid levels as well as from the restoration of normal sleep patterns. Collectively, these findings suggest that, although sleep deprivation inhibits adult neurogenesis by acting as a stressor, its compensatory aftereffects involve glucocorticoid-independent factors. dentate gyrus ͉ stress ͉ corticosterone ͉ cell proliferation ͉ adrenal steroids

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Section: Discussionmentioning

confidence: 95%

Section: Discussionmentioning

confidence: 98%

Sleep deprivation inhibits adult neurogenesis in the hippocampus by elevating glucocorticoids

Mirescu

Peters²,

Noiman³

et al. 2006

Proc. Natl. Acad. Sci. U.S.A.

204

137

View full text Add to dashboard Cite

show abstract

“…It is commonly used as a control for the confounding factors inherent to this technique. Although this control may be appropriate to address most of the confounding factors, it remains controversial (Landis 1996, Machado et al 2004. Indeed, when exposed to the MMPM, the animals placed on the wide platforms exhibit adrenal hypertrophy similar to that produced by placement on narrow platforms (Nunes and Tufik 1994a).…”

Section: Psd Methodsmentioning

confidence: 99%

“…Indeed, when exposed to the MMPM, the animals placed on the wide platforms exhibit adrenal hypertrophy similar to that produced by placement on narrow platforms (Nunes and Tufik 1994a). In addition, a wide platform induces some degree of PSD, as reflected by augmented rebound during the recovery period (Machado et al 2004). In the rotation disk method proposed by Rechtschaffen et al (1983), nonspecific concomitants of this technique are controlled by a "yoked" control animal, which is concurrently aroused with the experimental animal (Van Hulzen and Coenen 1979).…”

Section: Psd Methodsmentioning

confidence: 99%

Paradoxical sleep deprivation: neurochemical, hormonal and behavioral alterations. Evidence from 30 years of research

Tufik

Andersen

Bittencourt

et al. 2009

An. Acad. Bras. Ciênc.

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144

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Sleep comprises approximately one-third of a person's lifetime, but its impact on health and medical conditions remains partially unrecognized. The prevalence of sleep disorders is increasing in modern societies, with significant repercussions on people's well-being. This article reviews past and current literature on the paradoxical sleep deprivation method as well as data on its consequences to animals, ranging from behavioral changes to alterations in the gene expression. More specifically, we highlight relevant experimental studies and our group's contribution over the last three decades.

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“…Most of these studies monitored expression following SD and recovery sleep (RS) to distinguish circadian (time of day) from homeostatic influences. The stress produced from SD, however, is well documented [Meerlo et al, 2002;Machado et al, 2004]. Spontaneous sleep-wakefulness or natural sleep is less well studied, based on the short, rapid cycling of sleep-wake bouts in rodents, the requirement to dissociate circadian and homeostatic influences, and the possible effects on cellular activities resulting from the practical difficulty of sacrificing a sleeping animal without first waking him up.…”

mentioning

confidence: 99%

Rapid alterations in cortical protein profiles underlie spontaneous sleep and wake bouts

Vázquez

Hall

Witkowska

et al. 2008

J of Cellular Biochemistry

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Existing data indicate that sleep-wakefulness is an essential behavior. The biological function(s) of sleep, however, remains unknown, due, in part, to the lack of information available at the intracellular level. Preliminary microarray analyses show that changes in behavioral state influence regional mRNA profiles; however, the impact of sleep on protein signatures is virtually unexplored. In these studies, cortical protein profiles were examined after timed bouts of spontaneous sleep-wakefulness. Within minutes of each behavioral state examined, a small number of spots showing unique expression were detected. Mass spectroscopy analyses of sleep-and wake-related spots identified proteins associated with multiple functional categories. Two sleep-associated proteins were further validated using a sleep deprivation paradigm. We found preliminary evidence for two different post-transcriptional mechanisms-one (GAPDH) in which the amount of protein was increased in the recovery sleep following prolonged waking, while the other (actin) suggested that post-translational modifications may underlie sleep. The similarities between the effects of sleep on both protein and mRNA profiles indicate that dynamic intracellular changes underlie sleep-wake states and are consistent with roles for sleep in multiple biological functions. J. Cell. Biochem. 105: 1472Biochem. 105: -1484Biochem. 105: , 2008. ß 2008 Wiley-Liss, Inc. KEY WORDS: TWO-DIMENSIONAL ELECTROPHORESIS (2DE); MASS SPECTROMETRY; SPONTANEOUS SLEEP-WAKE BOUTS; SLEEP-ASSOCIATED PROTEIN EXPRESSIONS leep-wake behavior is a complex and tightly regulated Achermann, 1999, 2000] amalgam of physiological processes that involves reciprocal interactions between numerous brain regions that is coordinated by multiple neurotransmitter/peptide systems [Lin, 2000;Jones, 2004]. Sleep is exhibited by all animals studied thus far [Campbell and Tobler, 1984;Tobler, 2000] and constitutes a significant percentage of a 24 h period [Carskadon and Dement, 2000;Ohayon et al., 2004]. Alternations between sleep and wakefulness are regulated by a combination of circadian (sleep timing) [Edgar, 1995] and homeostatic factors (sleep need) [Borbely, 1982]. The homeostatic regulation of sleep is based on the observation that following sleep deprivation (SD), there is an increase in sleep time and intensity that is proportional to the sleep lost, suggesting that a need for sleep accumulates during waking in both rodents and humans [Tobler and Borbely, 1986;Riedner et al., 2007;Vyazovskiy et al., 2007]. In humans, SD results in marked cognitive and physiological impairments [Drummond and Brown, 2001;Durmer and Dinges, 2005], while prolonged SD in rats [Rechtschaffen, 1998] and flies [Shaw et al., 2002] is fatal. The biological function(s) of sleep, however, remains poorly characterized, though most agree that sleep serves a restorative function [Benington and Heller, 1995]. Proposed roles for sleep include the maintenance of body temperature [McGinty and Szymusiak, 1990;Wehr, 1992], energy ...

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Sleep deprivation induced by the modified multiple platform technique: quantification of sleep loss and recovery

Cited by 346 publications

References 31 publications

Sleep deprivation inhibits adult neurogenesis in the hippocampus by elevating glucocorticoids

Sleep deprivation inhibits adult neurogenesis in the hippocampus by elevating glucocorticoids

Paradoxical sleep deprivation: neurochemical, hormonal and behavioral alterations. Evidence from 30 years of research

Rapid alterations in cortical protein profiles underlie spontaneous sleep and wake bouts

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