Small platform sleep deprivation selectively increases the average duration of rapid eye movement sleep episodes during sleep rebound

Kitka, Tamás; Kátai, Zita; Pap, Dorottya; Molnár, Eszter; Ádori, Csaba; Bagdy, György

doi:10.1016/j.bbr.2009.08.004

Cited by 22 publications

(35 citation statements)

References 25 publications

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“…The results of cosinor analysis are consistent with those we report using other measures. Consistent with previous results in normal rats (30), NREMS, REMS and wake showed circadian distributions that fit a sine wave with a period of 24 h (P Ͻ 0.02) in B-SAP rats when food was available ad libitum. However, food restriction altered the cosinor fit in B-SAPs.…”

Section: Resultssupporting

confidence: 79%

Circadian integration of sleep-wake and feeding requires NPY receptor-expressing neurons in the mediobasal hypothalamus

Wiater

Mukherjee

et al. 2011

American Journal of Physiology-Regulatory, Integrative and Comp

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Sleep and feeding rhythms are highly coordinated across the circadian cycle, but the brain sites responsible for this coordination are unknown. We examined the role of neuropeptide Y (NPY) receptor-expressing neurons in the mediobasal hypothalamus (MBH) in this process by injecting the targeted toxin, NPY-saporin (NPY-SAP), into the arcuate nucleus (Arc). NPY-SAP-lesioned rats were initially hyperphagic, became obese, exhibited sustained disruption of circadian feeding patterns, and had abnormal circadian distribution of sleep-wake patterns. Total amounts of rapid eye movement sleep (REMS) and non-REMS (NREMS) were not altered by NPY-SAP lesions, but a peak amount of REMS was permanently displaced to the dark period, and circadian variation in NREMS was eliminated. The phase reversal of REMS to the dark period by the lesion suggests that REMS timing is independently linked to the function of MBH NPY receptor-expressing neurons and is not dependent on NREMS pattern, which was altered but not phase reversed by the lesion. Sleep-wake patterns were altered in controls by restricting feeding to the light period, but were not altered in NPY-SAP rats by restricting feeding to either the light or dark period, indicating that disturbed sleep-wake patterns in lesioned rats were not secondary to changes in food intake. Sleep abnormalities persisted even after hyperphagia abated during the static phase of the lesion. Results suggest that the MBH is required for the essential task of integrating sleep-wake and feeding rhythms, a function that allows animals to accommodate changeable patterns of food availability. NPY receptor-expressing neurons are key components of this integrative function. arcuate nucleus; NPY-saporin; obesity; rapid eye movement sleep FEEDING AND VIGILANCE (sleep-wake) states are rhythmically expressed across the circadian cycle, and their rhythms are highly integrated (3,64,75). Integration of sleep-wake and feeding rhythms is of fundamental importance for survival. Indeed, a wakeful state is an intrinsic requirement for feeding and foraging behavior, and, in a changeable environment, only close communication between these particular rhythms would permit an animal to respond adaptively and opportunistically to changing patterns of food availability. Although the suprachiasmatic nucleus of the hypothalamus (SCN) has an acknowledged role in establishing and maintaining circadian rhythms (47,63,83), including sleep-wake rhythms (15), entrainment of circadian food-anticipatory rhythms does not require the SCN (79,82), supporting the possibility that integration of sleep-wake and feeding also occurs outside the SCN. Furthermore, integration of physiological signals required to derive rhythms compatible with homeostatic requirements is likely to occur outside the SCN (6,48,75), as this arrangement would provide maximum flexibility for responding to varying challenges.Surprisingly few experiments have attempted to determine sites responsible for integration of sleep and feeding rhythms. However, a large body o...

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Section: Resultssupporting

confidence: 79%

Circadian integration of sleep-wake and feeding requires NPY receptor-expressing neurons in the mediobasal hypothalamus

Wiater

Mukherjee

et al. 2011

American Journal of Physiology-Regulatory, Integrative and Comp

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“…During the sleep rebound, caused by the mostly selective REMS deprivation, the REMS pressure predominates sleep, leading to a decrease in the amount of deep slow wave sleep and total slow wave sleep (Kitka et al 2009). Given the fact that REMS deprivation by the "flower pot" method also causes some slow wave sleep deprivation (Verret et al 2003) being much smaller in magnitude compared to REMS pressure, the existence of a slow wave sleep pressure is also feasible and suggested by rebound sleep data (Kitka et al 2009). As the SSRI treatment interferes with the high REMS pressure, we may conclude that the increased amount of deep slow wave sleep can be the consequence of the slight SWS deprivation.…”

Section: Discussionmentioning

confidence: 99%

“…After the habituation period, rats were detached from the electric cable and a 72-h-long REMS deprivation was performed as described earlier (Kitka et al 2009). Briefly, the HC animals were placed into single cages, and each RD animal was placed on a round platform (diameter = 6.5 cm, surface was 0.5 cm above the water level) situated in the middle of a round water tank (diameter= 41 cm).…”

Section: Rems Deprivation Proceduresmentioning

confidence: 99%

“…All animals were kept undisturbed, and food and water were available ad libitum during the REMS deprivation period. The "flower pot" sleep deprivation paradigm was established to be stressful for the animals; we addressed this question extensively in our previous papers (Kitka et al 2009(Kitka et al , 2011). The conclusion of our studies was that REM rebound and the activation of MCH neurons were strongly associated with each other, but not with stress.…”

Section: Rems Deprivation Proceduresmentioning

confidence: 99%

“…In order to exclude short REMS attempts, a REMS episode was defined as a period of REMS lasting for ≥16 s and not interrupted by ≥16 s of other vigilance states (Gandolfo et al 1996;Kitka et al 2009Kitka et al , 2011Vyazovskiy et al 2007). …”

Section: Eeg Recording and Evaluationmentioning

confidence: 99%

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Acute escitalopram treatment inhibits REM sleep rebound and activation of MCH-expressing neurons in the lateral hypothalamus after long term selective REM sleep deprivation

et al. 2013

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Rationale Selective rapid eye movement sleep (REMS) deprivation using the platform-on-water ("flower pot") method causes sleep rebound with increased REMS, decreased REMS latency, and activation of the melaninconcentrating hormone (MCH) expressing neurons in the hypothalamus. MCH is implicated in the pathomechanism of depression regarding its influence on mood, feeding behavior, and REMS. Objectives We investigated the effects of the most selective serotonin reuptake inhibitor escitalopram on sleep rebound following REMS deprivation and, in parallel, on the activation of MCH-containing neurons.Methods Escitalopram or vehicle (10 mg/kg, intraperitoneally) was administered to REMS-deprived (72 h) or home cage male Wistar rats. During the 3-h-long "rebound sleep", electroencephalography was recorded, followed by an MCH/Fos double immunohistochemistry. Results During REMS rebound, the time spent in REMS and the number of MCH/Fos double-labeled neurons in the lateral hypothalamus increased markedly, and REMS latency showed a significant decrease. All these effects of REMS deprivation were significantly attenuated by escitalopram treatment. Besides the REMS-suppressing effects, escitalopram caused an increase in amount of and decrease in latency of slow wave sleep during the rebound. Conclusions These results show that despite the high REMS pressure caused by REMS deprivation procedure, escitalopram has the ability to suppress REMS rebound, as well as to diminish the activation of MCH-containing neurons, in parallel. Escitalopram caused a shift from REMS to slow wave sleep during the rebound. Furthermore, these data point to the potential connection between the serotonergic system and MCH in sleep regulation, which can be relevant in depression and in other mood disorders.

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Exploring the role of neuropeptide S in the regulation of arousal: a functional anatomical study

et al. 2015

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Neuropeptide S (NPS) is a regulatory peptide expressed by limited number of neurons in the brainstem. The simultaneous anxiolytic and arousal-promoting effect of NPS suggests an involvement in mood control and vigilance, making the NPS-NPS receptor system an interesting potential drug target. Here we examined, in detail, the distribution of NPS-immunoreactive (IR) fiber arborizations in brain regions of rat known to be involved in the regulation of sleep and arousal. Such nerve terminals were frequently apposed to GABAergic/galaninergic neurons in the ventro-lateral preoptic area (VLPO) and to tyrosine hydroxylase-IR neurons in all hypothalamic/thalamic dopamine cell groups. Then we applied the single platform-on-water (mainly REM) sleep deprivation method to study the functional role of NPS in the regulation of arousal. Of the three pontine NPS cell clusters, the NPS transcript levels were increased only in the peri-coerulear group in sleep-deprived animals, but not in stress controls. The density of NPS-IR fibers was significantly decreased in the median preoptic nucleus-VLPO region after the sleep deprivation, while radioimmunoassay and mass spectrometry measurements showed a parallel increase of NPS in the anterior hypothalamus. The expression of the NPS receptor was, however, not altered in the VLPO-region. The present results suggest a selective activation of one of the three NPS-expressing neuron clusters as well as release of NPS in distinct forebrain regions after sleep deprivation. Taken together, our results emphasize a role of the peri-coerulear cluster in the modulation of arousal, and the importance of preoptic area for the action of NPS on arousal and sleep.

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Small platform sleep deprivation selectively increases the average duration of rapid eye movement sleep episodes during sleep rebound

Cited by 22 publications

References 25 publications

Circadian integration of sleep-wake and feeding requires NPY receptor-expressing neurons in the mediobasal hypothalamus

Circadian integration of sleep-wake and feeding requires NPY receptor-expressing neurons in the mediobasal hypothalamus

Acute escitalopram treatment inhibits REM sleep rebound and activation of MCH-expressing neurons in the lateral hypothalamus after long term selective REM sleep deprivation

Exploring the role of neuropeptide S in the regulation of arousal: a functional anatomical study

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