No loss of orexin/hypocretin, melanin‐concentrating hormone, or locus coeruleus noradrenergic neurons in a rat model of chronic sleep restriction

Author(s):  
Samuel Deurveilher ◽  
Michael Antonchuk ◽  
Brock St. C. Saumure ◽  
Andrew Baldin ◽  
Kazue Semba
SLEEP ◽  
2020 ◽  
Vol 43 (11) ◽  
Author(s):  
Shannon Hall ◽  
Samüel Deurveilher ◽  
George S Robertson ◽  
Kazue Semba

Abstract Chronic sleep restriction (CSR) negatively impacts brain functions. Whether microglia, the brain’s resident immune cells, play any role is unknown. We studied microglia responses to CSR using a rat model featuring slowly rotating wheels (3 h on/1 h off), which was previously shown to induce both homeostatic and adaptive responses in sleep and attention. Adult male rats were sleep restricted for 27 or 99 h. Control rats were housed in locked wheels. After 27 and/or 99 h of CSR, the number of cells immunoreactive for the microglia marker ionized calcium-binding adaptor molecule-1 (Iba1) and the density of Iba1 immunoreactivity were increased in 4/10 brain regions involved in sleep/wake regulation and cognition, including the prelimbic cortex, central amygdala, perifornical lateral hypothalamic area, and dorsal raphe nucleus. CSR neither induced mitosis in microglia (assessed with bromodeoxyuridine) nor impaired blood–brain barrier permeability (assessed with Evans Blue). Microglia appeared ramified in all treatment groups and, when examined quantitatively in the prelimbic cortex, their morphology was not affected by CSR. After 27 h, but not 99 h, of CSR, mRNA levels of the anti-inflammatory cytokine interleukin-10 were increased in the frontal cortex. Pro-inflammatory cytokine mRNA levels (tumor necrosis factor-α, interleukin-1β, and interleukin-6) were unchanged. Furthermore, cortical microglia were not immunoreactive for several pro- and anti-inflammatory markers tested, but were immunoreactive for the purinergic P2Y12 receptor. These results suggest that microglia respond to CSR while remaining in a physiological state and may contribute to the previously reported homeostatic and adaptive responses to CSR.


2017 ◽  
Vol 66 ◽  
pp. e16
Author(s):  
S.E. Hall ◽  
S. Deurveilher ◽  
K. Semba

2021 ◽  
Author(s):  
Ali-Mohammad Kamali ◽  
Fatemeh Karimi ◽  
Ali Noorafshan ◽  
Azam Soleimani ◽  
Saied Karbalay-Doust ◽  
...  

UNSTRUCTURED This study examined the consequences of chronic sleep restriction (CSR) with or without curcumin treatment on quantitative histomorphological correlates of the locus coeruleus (LC) nucleus using stereological techniques. Male rats were assigned to five groups including: 1-control (C), 2- curcumin (CUR), 3- grid floor (GF), 4- CSR and 5- CSR+ curcumin (CUR) (100 mg/kg/day). Animals in the GF group were placed on wire-mesh grids while in the CSR box (modified multiple platform paradigm). After a period of 21 days, rats were sacrificed with their brains excised and assessed using stereological procedures. Our findings revealed a 22%, 45% and 47% reduction in the total volume, the total number of neurons and glial cells of LC in CSR group as compared to the control groups, respectively (p < 0.01). Such structural changes were abrogated in the CSR+CUR compared to the CSR group. The study outcome proposed potential neuroprotective effects of CUR in our sleep-restricted rat model. Further translational approaches would shed more light on the possible clinical significance of such finding in human subjects with chronic sleep loss including those with intensive shift-work schedules.


SLEEP ◽  
2017 ◽  
Vol 40 (8) ◽  
Author(s):  
Ali-Mohammad Kamali ◽  
Ali Noorafshan ◽  
Fatemeh Karimi ◽  
Saied Karbalay-Doust ◽  
Mohammad Nami

SLEEP ◽  
2020 ◽  
Author(s):  
Erika M Yamazaki ◽  
Caroline A Antler ◽  
Charlotte R Lasek ◽  
Namni Goel

Abstract Study Objectives The amount of recovery sleep needed to fully restore well-established neurobehavioral deficits from sleep loss remains unknown, as does whether the recovery pattern differs across measures after total sleep deprivation (TSD) and chronic sleep restriction (SR). Methods In total, 83 adults received two baseline nights (10–12-hour time in bed [TIB]) followed by five 4-hour TIB SR nights or 36-hour TSD and four recovery nights (R1–R4; 12-hour TIB). Neurobehavioral tests were completed every 2 hours during wakefulness and a Maintenance of Wakefulness Test measured physiological sleepiness. Polysomnography was collected on B2, R1, and R4 nights. Results TSD and SR produced significant deficits in cognitive performance, increases in self-reported sleepiness and fatigue, decreases in vigor, and increases in physiological sleepiness. Neurobehavioral recovery from SR occurred after R1 and was maintained for all measures except Psychomotor Vigilance Test (PVT) lapses and response speed, which failed to completely recover. Neurobehavioral recovery from TSD occurred after R1 and was maintained for all cognitive and self-reported measures, except for vigor. After TSD and SR, R1 recovery sleep was longer and of higher efficiency and better quality than R4 recovery sleep. Conclusions PVT impairments from SR failed to reverse completely; by contrast, vigor did not recover after TSD; all other deficits were reversed after sleep loss. These results suggest that TSD and SR induce sustained, differential biological, physiological, and/or neural changes, which remarkably are not reversed with chronic, long-duration recovery sleep. Our findings have critical implications for the population at large and for military and health professionals.


SLEEP ◽  
2021 ◽  
Author(s):  
Jelena Skorucak ◽  
Nathan Weber ◽  
Mary A Carskadon ◽  
Chelsea Reynolds ◽  
Scott Coussens ◽  
...  

Abstract The high prevalence of chronic sleep restriction in adolescents underscores the importance of understanding how adolescent sleep is regulated under such conditions. One component of sleep regulation is a homeostatic process: if sleep is restricted, then sleep intensity increases. Our knowledge of this process is primarily informed by total sleep deprivation studies and has been incorporated in mathematical models of human sleep regulation. Several animal studies, however, suggest that adaptation occurs in chronic sleep restriction conditions, showing an attenuated or even decreased homeostatic response. We investigated the homeostatic response of adolescents to different sleep opportunities. Thirty-four participants were allocated to one of three groups with 5, 7.5 or 10 h of sleep opportunity per night for 5 nights. Each group underwent a protocol of 9 nights designed to mimic a school week between 2 weekends: 2 baseline nights (10 h sleep opportunity), 5 condition nights (5, 7.5 or 10 h), and two recovery nights (10 h). Measures of sleep homeostasis (slow-wave activity and slow-wave energy) were calculated from frontal and central EEG derivations and compared to predictions derived from simulations of the homeostatic process of the two-process model of sleep regulation. Only minor differences were found between empirical data and model predictions, indicating that sleep homeostasis is preserved under chronic sleep restriction in adolescents. These findings improve our understanding of effects of repetitive short sleep in adolescents.


2020 ◽  
Vol 10 (1) ◽  
Author(s):  
Xiangdong Du ◽  
Ming Yin ◽  
Lian Yuan ◽  
Guangya Zhang ◽  
Yan Fan ◽  
...  

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