Curcumin to abrogate structural changes in the locus coeruleus following chronic sleep restriction in rats (Preprint)

2021 ◽  
Author(s):  
Ali-Mohammad Kamali ◽  
Fatemeh Karimi ◽  
Ali Noorafshan ◽  
Azam Soleimani ◽  
Saied Karbalay-Doust ◽  
...  
Keyword(s):  
Locus Coeruleus ◽  
Structural Changes ◽  
Human Subjects ◽  
Grid Floor ◽  
Wire Mesh ◽  
Male Rats ◽  
Sleep Restriction ◽  
Neuroprotective Effects ◽  
Multiple Platform ◽  
Chronic Sleep

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.

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

2021 ◽  
Author(s):  
Samuel Deurveilher ◽  
Michael Antonchuk ◽  
Brock St. C. Saumure ◽  
Andrew Baldin ◽  
Kazue Semba
Keyword(s):  
Locus Coeruleus ◽  
Rat Model ◽  
Sleep Restriction ◽  
Noradrenergic Neurons ◽  
Melanin Concentrating Hormone ◽  
Chronic Sleep

scholarly journals Homeostatic state of microglia in a rat model of chronic sleep restriction

SLEEP ◽  
2020 ◽  
Vol 43 (11) ◽  
Author(s):  
Shannon Hall ◽  
Samüel Deurveilher ◽  
George S Robertson ◽  
Kazue Semba
Keyword(s):  
Rat Model ◽  
Inflammatory Cytokine ◽  
Male Rats ◽  
Sleep Restriction ◽  
Mrna Levels ◽  
Prelimbic Cortex ◽  
Adaptive Responses ◽  
Brain Functions ◽  
Anti Inflammatory ◽  
Chronic Sleep

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.

Transcriptional alterations of genes related to fertility decline in male rats induced by chronic sleep restriction

2020 ◽  
Vol 66 (2) ◽  
pp. 99-111 ◽  
Author(s):  
Wenyang Chen ◽  
Xingdao Guo ◽  
Zhiping Jin ◽  
Runan Li ◽  
Lixia Shen ◽  
...  
Keyword(s):  
Fertility Decline ◽  
Male Rats ◽  
Sleep Restriction ◽  
Transcriptional Alterations ◽  
Chronic Sleep

scholarly journals Effects of Chronic REM Sleep Restriction on D1Receptor and Related Signal Pathways in Rat Prefrontal Cortex

2015 ◽  
Vol 2015 ◽  
pp. 1-9 ◽  
Author(s):  
Yan Han ◽  
Xiaosa Wen ◽  
Fei Rong ◽  
Xinmin Chen ◽  
Ruying Ouyang ◽  
...  
Keyword(s):  
Prefrontal Cortex ◽  
Rem Sleep ◽  
Molecular Mechanisms ◽  
Sleep Restriction ◽  
Signal Pathways ◽  
Neural Function ◽  
Multiple Platform ◽  
Pka Pathway ◽  
Chronic Sleep ◽  
Neural Dysfunction

The prefrontal cortex (PFC) mediates cognitive function that is sensitive to disruption by sleep loss, and molecular mechanisms regulating neural dysfunction induced by chronic sleep restriction (CSR), particularly in the PFC, have yet to be completely understood. The aim of the present study was to investigate the effect of chronic REM sleep restriction (REM-CSR) on the D1receptor (D1R) and key molecules in D1R’ signal pathways in PFC. We employed the modified multiple platform method to create the REM-CSR rat model. The ultrastructure of PFC was observed by electron microscopy. HPLC was performed to measure the DA level in PFC. The expressions of genes and proteins of related molecules were assayed by real-time PCR and Western blot, respectively. The general state and morphology of PFC in rats were changed by CSR, and DA level and the expression of D1R in PFC were markedly decreased (P<0.01,P<0.05); the expression of phosphor-PKAcαwas significantly lowered in CSR rats (P<0.05). The present results suggested that the alteration of neuropathology and D1R expression in PFC may be associated with CSR induced cognitive dysfunction, and the PKA pathway of D1R may play an important role in the impairment of advanced neural function.

Time-of-day modulation of homeostatic and allostatic sleep responses to chronic sleep restriction in rats

2012 ◽  
Vol 302 (12) ◽  
pp. R1411-R1425 ◽  
Author(s):  
S. Deurveilher ◽  
B. Rusak ◽  
K. Semba
Keyword(s):  
Eye Movement ◽  
Recovery Period ◽  
Sleep Time ◽  
Time Of Day ◽  
Male Rats ◽  
Sleep Restriction ◽  
Rapid Eye Movement ◽  
Rapid Eye Movement Sleep ◽  
Delta Power ◽  
Chronic Sleep

To study sleep responses to chronic sleep restriction (CSR) and time-of-day influences on these responses, we developed a rat model of CSR that takes into account the polyphasic sleep patterns in rats. Adult male rats underwent cycles of 3 h of sleep deprivation (SD) and 1 h of sleep opportunity (SO) continuously for 4 days, beginning at the onset of the 12-h light phase (“3/1” protocol). Electroencephalogram (EEG) and electromyogram (EMG) recordings were made before, during, and after CSR. During CSR, total sleep time was reduced by ∼60% from baseline levels. Both rapid eye movement sleep (REMS) and non-rapid eye movement sleep (NREMS) during SO periods increased initially relative to baseline and remained elevated for the rest of the CSR period. In contrast, NREMS EEG delta power (a measure of sleep intensity) increased initially, but then declined gradually, in parallel with increases in high-frequency power in the NREMS EEG. The amplitude of daily rhythms in NREMS and REMS amounts was maintained during SO periods, whereas that of NREMS delta power was reduced. Compensatory responses during the 2-day post-CSR recovery period were either modest or negative and gated by time of day. NREMS, REMS, and EEG delta power lost during CSR were not recovered by the end of the second recovery day. Thus the “3/1” CSR protocol triggered both homeostatic responses (increased sleep amounts and intensity during SOs) and allostatic responses (gradual decline in sleep intensity during SOs and muted or negative post-CSR sleep recovery), and both responses were modulated by time of day.

Chronic Sleep Restriction Outcome on the Volumetric Correlates, Neuronal and Glial Number of the Hypoglossal Nucleus in a Rat Model (Preprint)

2021 ◽  
Author(s):  
Fatemeh Karimi ◽  
Ali-Mohammad Kamali ◽  
Ali Noorafshan ◽  
Saied Karbalay-Doust ◽  
KS Rao ◽  
...  
Keyword(s):  
Brain Stem ◽  
Glial Cells ◽  
Male Rats ◽  
Sleep Restriction ◽  
Hypoglossal Nucleus ◽  
Airway Patency ◽  
Cage Control ◽  
Obstructive Sleep ◽  
The Brain ◽  
Chronic Sleep

BACKGROUND Chronic sleep restriction (CSR) is known to result in various changes in brain structures including the dorsal respiratory nuclei of the brain stem. Obstructive sleep apnea has partly been resulted from reduced tone of the muscles including the tongue which are involved in maintaining airway patency during sleep. OBJECTIVE This study aimed at investigating whether CSR may result in structural changes in the hypoglossal nerve nuclei. METHODS Three groups of male rats (each comprising 6) were randomly assigned to CSR, cage control and grid-floor control groups. CSR was imposed using the modified multi-platform box containing water for 18 hours/day for 21 days. At the end of 21 days, the rats’ brain was removed and stained through the modified Giemsa method. The hypoglossal nucleus (HGN) was evaluated through stereological approach. RESULTS The volume of HGN as well as the total number of neuronal and glial cells did not show significant differences between the cage control and the other groups (p=0.3). CONCLUSIONS The current study provided evidence to support that CSR induced by the modified multiple platform approach for 18 hours/day over 21 days in rats, neither results in volume reduction, nor neuronal and glial cells loss in the hypoglossal nuclei in the brain stem.

Fine Structural Changes in the Adenohypophyses of Rats Following Destruction of the Pituitary Stalk

1977 ◽  
Vol 35 ◽  
pp. 496-497
Author(s):  
K. Kovacs ◽  
E. Horvath ◽  
J. M. Bilbao ◽  
F. A. Laszlo ◽  
I. Domokos
Keyword(s):  
Structural Changes ◽  
Tissue Injury ◽  
Anterior Lobe ◽  
Uranyl Acetate ◽  
Male Rats ◽  
Pituitary Stalk ◽  
Sequence Of Events ◽  
Pituitary Glands ◽  
Electrolytic Lesions ◽  
Ultrathin Sections

Electrolytic lesions of the pituitary stalk in rats interrupt adenohypophysial blood flow and result in massive infarction of the anterior lobe. In order to obtain a deeper insight into the morphogenesis of tissue injury and to reveal the sequence of events, a fine structural investigation was undertaken on adenohypophyses of rats at various intervals following destruction of the pituitary stalk.The pituitary stalk was destroyed electrolytically, with a Horsley-Clarke apparatus on 27 male rats of the R-Amsterdam strain, weighing 180-200 g. Thirty minutes, 1,2,4,6 and 24 hours after surgery the animals were perfused with a glutaraldehyde-formalin solution. The skulls were then opened and the pituitary glands removed. The anterior lobes were fixed in glutaraldehyde-formalin solution, postfixed in osmium tetroxide and embedded in Durcupan. Ultrathin sections were stained with uranyl acetate and lead citrate and investigated with a Philips 300 electron microscope.

Berberine nanoencapsulation attenuates hallmarks of scoplomine induced Alzheimer's-like disease in rats

2020 ◽  
Vol 15 ◽  
Author(s):  
Samar R. Saleh ◽  
Mariam M. Abady ◽  
Mohammed Nofal ◽  
Nashwa W. Yassa ◽  
Mohamed S. Abdel-latif ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Histopathological Examination ◽  
Memory Function ◽  
Amyloid Β ◽  
Active Pharmaceutical Ingredient ◽  
Isoquinoline Alkaloid ◽  
Drug Uptake ◽  
Male Rats ◽  
Morris Water Maze Test ◽  
Neuroprotective Effects

Background: Berberine (BBR), an isoquinoline alkaloid, acts as a multipotent active pharmaceutical ingredient to counteract several types of dementia based on its numerous pharmacological actions including antioxidant, antiinflammatory, cholesterol-lowering effect, and inhibition of Aβ production and AChE. However, BBR suffers from poor absorption, bioavailability and brain drug uptake. The present study is directed for the formulation and characterization of Chitosan BBR-nanoparticles (BBR-NPs) as well as the estimation of its neuroprotective effects against scopolamine induced cognitive impairments. Methods: BBR-NPs were formulated using ionic gelation method and tripolyphosphate was chosen as a cross linker. Nanoparticles size, zeta potential, encapsulation efficiency and releasing profile were estimated. To investigate the neuroprotective effects, adult fifty six Wistar male rats were randomly distributed into: three control groups, received saline, polyethylene glycol or chitosan- NPs respectively; induced group, received scopolamine (2 mg/ kg, i.p.) and three treated groups were orally administrated BBR (50 mg/ kg), BBR- NP (7 mg/ kg) and donepezil (2.25 mg/ kg, as positive control) followed by scopolamine injection after 40 min, daily for 4 weeks. Morris water maze test, oxidative stress parameters, cholinergic and amyloid-β processing intermediates as well as neuroplasticity markers and histopathological examination were assessed. Results: Our results showed that BBR- NPs were better than BBR and donepezil as BBR- NPs were powerful inhibitory ligands toward AChE and Aβ42 formation and significantly down regulated Tau, iNOS and BACE gene expression in rats’ hippocampus. BBR-NPs administration, at 1/6 of BBR therapeutic recommended dose, significantly improved learning and memory function. This could be accredited to the diminution of oxidative stress and amyloid-β toxicity in addition to the improvement of the neuroplasticity markers. Conclusions: The enhancing effect of BBR- NPs could be related to the enhancing of its bioavailability, absorption and brain drug uptake which need more investigation in future work.

scholarly journals Residual, differential neurobehavioral deficits linger after multiple recovery nights following chronic sleep restriction or acute total sleep deprivation

SLEEP ◽  
2020 ◽  
Author(s):  
Erika M Yamazaki ◽  
Caroline A Antler ◽  
Charlotte R Lasek ◽  
Namni Goel
Keyword(s):  
Sleep Deprivation ◽  
Response Speed ◽  
Sleep Loss ◽  
Sleep Restriction ◽  
Total Sleep Deprivation ◽  
Psychomotor Vigilance Test ◽  
Recovery Sleep ◽  
Time In Bed ◽  
Neurobehavioral Deficits ◽  
Chronic Sleep

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.

Homeostatic Response to Sleep Restriction in Adolescents

SLEEP ◽  
2021 ◽  
Author(s):  
Jelena Skorucak ◽  
Nathan Weber ◽  
Mary A Carskadon ◽  
Chelsea Reynolds ◽  
Scott Coussens ◽  
...  
Keyword(s):  
Slow Wave ◽  
Process Model ◽  
Animal Studies ◽  
Sleep Restriction ◽  
Sleep Regulation ◽  
Homeostatic Process ◽  
Sleep Homeostasis ◽  
High Prevalence ◽  
Homeostatic Response ◽  
Chronic Sleep

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.

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