The effect of slow wave sleep deprivation on mood in adolescents with depressive symptoms: A pilot study

Palatine, Elise; Phillips, Mary L.; Soehner, Adriane M.

doi:10.1016/j.jad.2024.03.058

Cited by 1 publication

(1 citation statement)

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“… 3 Especially in the intensive care unit (ICU), 59–80% of ICU patients experience sleep disruptions such as sleep latency, fragmentation and circadian rhythm disturbances, 4 , 5 which are even in ICU patient survivors for at least 12 months. 6 The physical and psychological effects of sleep deprivation (SD) include cognitive impairment, 7 anxiety, 8 depression, 9 systemic inflammation, 10 and oxidative stress. 8 Besides, SD is closely associated with other common ICU complications, such as delirium.…”

Section: Introductionmentioning

confidence: 99%

Propofol improves sleep deprivation‐induced sleep structural and cognitive deficits via upregulating the BMAL1 expression and suppressing microglial M1 polarization

Liu,

Yang,

Wang

et al. 2024

CNS Neurosci Ther

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BackgroundSleep deprivation (SD) is a growing global health problem with many deleterious effects, such as cognitive impairment. Microglia activation‐induced neuroinflammation may be an essential factor in this. Propofol has been shown to clear sleep debt after SD in rats. This study aims to evaluate the effects of propofol‐induced sleep on ameliorating sleep quality impairment and cognitive decline after 48 h SD.MethodsAlmost 8–12‐week‐old rats were placed in the SD system for 48 h of natural sleep or continuous SD. Afterwards, rats received propofol (20 mg·kg−1·h−1, 6 h) via the tail or slept naturally. The Morris water maze (MWM) and Y‐maze test assessed spatial learning and memory abilities. Rat EEG/EMG monitored sleep. The expression of brain and muscle Arnt‐like protein 1 (BMAL1), brain‐derived neurotrophic factor (BDNF) in the hippocampus and BMAL1 in the hypothalamus were assessed by western blot. Enzyme‐linked immunosorbent assay detected IL‐6, IL‐1β, arginase 1 (Arg1), and IL‐10 levels in the hippocampus. Immunofluorescence was used to determine microglia expression as well as morphological changes.ResultsCompared to the control group, the sleep‐deprived rats showed poor cognitive performance on both the MWM test and the Y‐maze test, accompanied by disturbances in sleep structure, including increased total sleep time, and increased time spent and delta power in non‐rapid eye movement sleep. In addition, SD induces abnormal expression of the circadian rhythm protein BMAL1, activates microglia, and causes neuroinflammation and nerve damage. Propofol reversed these changes and saved sleep and cognitive impairment. Furthermore, propofol treatment significantly reduced hippocampal IL‐1β and IL‐6 levels, increased BDNF, Arg1, and IL‐10 levels, and switched microglia surface markers from the inflammatory M1 type to the anti‐inflammatory M2 type.ConclusionPropofol reduces SD‐induced cognitive impairment and circadian rhythm disruption, possibly by lowering neuronal inflammation and switching the microglia phenotype from an M1 to an M2 activated state, thus exerting neuroprotective effects.

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