Effects of sleep deprivation and recovery sleep upon cell proliferation in adult rat dentate gyrus

Tung, Avery; Takase, Luiz Fernando; Fornal, Casimir A.; Jacobs, Barry L.

doi:10.1016/j.neuroscience.2005.06.008

Cited by 78 publications

(61 citation statements)

References 8 publications

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“…after prolonged sleep deprivation, which is characterized by an overshoot in the amount of sleep, is not temporally associated with an increase in cell proliferation. Instead, the period of sleep rebound coincides with a continued suppression of cell proliferation (14), which resembles the pattern observed after acute stress exposure (32). Furthermore, previous studies that have experimentally reduced CORT levels to the low physiological range have not reported increases in cell proliferation (33,34).…”

Section: Discussionsupporting

confidence: 56%

“…The reduction of cell proliferation and adult neurogenesis has also been shown in previous studies by using different methods of sleep deprivation, such as the treadmill and disk-over-water methods (14)(15)(16)(17). With the disk-over-water paradigm, animals are motivated to remain awake, because continued sleep runs the risk of falling into water; animals can escape this consequence if they move with the rotating disk.…”

Section: Discussionmentioning

confidence: 61%

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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: Discussionsupporting

confidence: 56%

Section: Discussionmentioning

confidence: 61%

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

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“…We have previously seen this following 56 hours of sleep deprivation (Tung et al, 2005) and following neurotoxic lesions of the median raphe (Sundararaman, 2006). The significance of this lies in the possibility that the dorsal hippocampus is more importantly involved in spatial learning and that the ventral hippocampus is more importantly involved in visceral learning (Moser & Moser, 1998;Faure et al, 2006).…”

Section: Discussionmentioning

confidence: 77%

Delayed suppression of hippocampal cell proliferation in rats following inescapable shocks

Fornal¹,

Stevens²,

Barson³

et al. 2007

Brain Research

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Adult Sprague-Dawley rats were exposed to a single session of 100 inescapable tail shocks (IS). Bromodeoxyuridine (BrdU) was administered 1 h, 2 d or 7 d later and hippocampal cell proliferation (CP) was assessed after a two-hour survival period. Measures of plasma corticosterone (CORT) levels were also obtained. Despite a large increase in CORT immediately following IS, no associated change in CP was observed. In fact, the only significant change in CP was seen 7 days after IS, at a time when CORT was unchanged from control levels. These data raise questions about the general nature of the relationship between CORT and CP. They also suggest that, under some conditions, changes in hippocampal CP may emerge only after an "incubation period".

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“…We have recently used the RSR paradigm to demonstrate that rats allowed to sleep for only 4 h per day for 8 consecutive days have increased basal corticosterone levels and develop pronounced changes in the reactivity of the hypothalamo-pituitary-adrenal axis to stress (18). RSR and other forms of SD have also been shown to alter regulation of corticosterone (18)(19)(20) and proinflammatory cytokine levels (21,22), elevate markers of oxidative stress (23), and promote neurodegenerative processes in the hippocampus (24,25).…”

Section: Discussionmentioning

confidence: 99%

Repeated sleep restriction in rats leads to homeostatic and allostatic responses during recovery sleep

Kim

Laposky

Bergmann

et al. 2007

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

114

108

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Recent studies indicate that chronic sleep restriction can have negative consequences for brain function and peripheral physiology and can contribute to the allostatic load throughout the body. Interestingly, few studies have examined how the sleep-wake system itself responds to repeated sleep restriction. In this study, rats were subjected to a sleep-restriction protocol consisting of 20 h of sleep deprivation (SD) followed by a 4-h sleep opportunity each day for 5 consecutive days. In response to the first 20-h SD block on day 1, animals responded during the 4-h sleep opportunity with enhanced sleep intensity [i.e., nonrapid eye movement (NREM) delta power] and increased rapid eye movement sleep time compared with baseline. This sleep pattern is indicative of a homeostatic response to acute sleep loss. Remarkably, after the 20-h SD blocks on days 2-5, animals failed to exhibit a compensatory NREM delta power response during the 4-h sleep opportunities and failed to increase NREM and rapid eye movement sleep times, despite accumulating a sleep debt each consecutive day. After losing Ϸ35 h of sleep over 5 days of sleep restriction, animals regained virtually none of their lost sleep, even during a full 3-day recovery period. These data demonstrate that the compensatory/ homeostatic sleep response to acute SD does not generalize to conditions of chronic partial sleep loss. We propose that the change in sleep-wake regulation in the context of repeated sleep restriction reflects an allostatic process, and that the allostatic load produced by SD has direct effects on the sleep-wake regulatory system. allostasis ͉ homeostasis ͉ sleep deprivation ͉ stress ͉ rodents

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Effects of sleep deprivation and recovery sleep upon cell proliferation in adult rat dentate gyrus

Cited by 78 publications

References 8 publications

Sleep deprivation inhibits adult neurogenesis in the hippocampus by elevating glucocorticoids

Sleep deprivation inhibits adult neurogenesis in the hippocampus by elevating glucocorticoids

Delayed suppression of hippocampal cell proliferation in rats following inescapable shocks

Repeated sleep restriction in rats leads to homeostatic and allostatic responses during recovery sleep

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