Alterations of sleep deprivation on brain function:A coordinatebased resting-state functional magnetic resonance imaging metaanalysis

BACKGROUND Sleep deprivation is a prevalent issue that impacts cognitive function.Although numerous neuroimaging studies have explored the neural correlates of sleep loss,inconsistencies persist in the reported results,necessitating an investigation into the consistent brain functional changes resulting from sleep loss.AIM To establish the consistency of brain functional alterations associated with sleep deprivation through systematic searches of neuroimaging databases.Two metaanalytic methods,signed differential mapping(SDM)and activation likelihood estimation(ALE),were employed to analyze functional magnetic resonance imaging(fMRI)data.METHODS A systematic search performed according to PRISMA guidelines was conducted across multiple databases through July 29,2023.Studies that met specific inclusion criteria,focused on healthy subjects with acute sleep deprivation and reported whole-brain functional data in English were considered.A total of 21 studies were selected for SDM and ALE meta-analyses.RESULTS Twenty-one studies,including 23 experiments and 498 subjects,were included.Compared to pre-sleep deprivation,post-sleep deprivation brain function was associated with increased gray matter in the right corpus callosum and decreased activity in the left medial frontal gyrus and left inferior parietal lobule.SDM revealed increased brain functional activity in the left striatum and right central posterior gyrus and decreased activity in the right cerebellar gyrus,left middle frontal gyrus,corpus callosum,and right cuneus.CONCLUSION This meta-analysis consistently identified brain regions affected by sleep deprivation,notably the left medial frontal gyrus and corpus callosum,shedding light on the neuropathology of sleep deprivation and offering insights into its neurological impact.

Overexpression of Sirt6 ameliorates sleep deprivation induced-cognitive impairment by modulating glutamatergic neuron function

Sleep benefits the restoration of energy metabolism and thereby suppo rts neuronal plasticity and cognitive behaviors.Sirt6 is a NAD+-dependent protein deacetylase that has been recognized as an essential regulator of energy metabolism because it modulates various transcriptional regulators and metabolic enzymes.The aim of this study was to investigate the influence of Sirt6 on cerebral function after chronic sleep deprivation(CSD).We assigned C57BL/6J mice to control or two CSD groups and subjected them to AAV2/9-CMV-EGFP or AAV2/9-CMV-Sirt6-EGFP infection in the prelimbic cortex(PrL).We then assessed cerebral functional connectivity(FC) using resting-state functional MRI,neuron/astrocyte metabolism using a metabolic kinetics analysis;dendritic spine densities using sparse-labeling;and miniature excitato ry postsynaptic currents(mEPSCs) and action potential(AP) firing rates using whole-cell patchclamp recordings.In addition,we evaluated cognition via a comprehensive set of behavioral tests.Compared with controls,Sirt6 was significantly decreased(P<0.05) in the PrL after CSD,accompanied by cognitive deficits and decreased FC between the PrL and accumbens nucleus,piriform cortex,motor co rtex,somatosensory co rtex,olfactory tubercle,insular cortex,and cerebellum.Sirt6 ove rexpression reve rsed CSD-induced cognitive impairment and reduced FC.Our analysis of metabolic kinetics using [1-13C] glucose and [2-13C] acetate showed that CSD reduced neuronal Glu4and GABA2synthesis,which could be fully restored via forced Sirt6 expression.Furthermore,Sirt6 ove rexpression reversed CSD-induced decreases in AP firing rates as well as the frequency and amplitude of mEPSCs in PrL pyramidal neurons.These data indicate that Sirt6 can improve cognitive impairment after CSD by regulating the PrL-associated FC network,neuronal glucose metabolism,and glutamatergic neurotransmission.Thus,Sirt6 activation may have potential as a novel strategy for treating sleep disorder-related diseases.

nfluence of paradoxical sleep deprivation and sleep recovery on testosterone level in rats of different ages

This study was performed to assess serum testosterone alterations induced by paradoxical sleep deprivation （PSD） and to verify their attenuation during sleep recovery （SR） based on different durations and ages. Wistar male rats aged 12 weeks for the younger group and 20 weeks for the elder group were randomly distributed into one of the following groups： a control group （cage and platform）, 3-day SD, 5-day SD, 7-day SD, 1-day SR, 3-day SR and 5-day SR groups. For PSD, the modified multiple platform method was used to specifically limit rapid eye movement （REM） sleep. Differences in the testosterone and luteinizing hormone levels between the younger group and the elder group according to duration of PSD and SR recovery were analysed. Testosterone continued to fall during the sleep deprivation period in a time-dependent manner in both the younger （P=-0.001, correlation coefficient r=-0.651） and elder groups （P=0.001, correlation coefficient r=-0.840）. The elder group showed a significantly lower level of testosterone compared with the younger group after PSD. Upon SR after 3 days of PSD, the testosterone level continued to rise for 5 days after sleep recovery in the younger group （P=0.013）, whereas testosterone concentrations failed to recover until day 5 in the elder group. PSD caused a more detrimental effect on serum testosterone in the elder group compared to the younger group with respect to decreases in luteinizing hormone （LH） levels. The replenishment of serum testosterone level was prohibited in the elder group suggesting that the effects of SD/SR may be age-dependent. The mechanism by which SD affects serum testosterone and how age may modify the process are still unclear.

Progressive paradoxical sleep deprivation impairs partial memory following learning tasks in rats

BACKGROUND： Complex learning tasks result in a greater number of paradoxical sleep phases, which can improve memory. The effect of paradoxical sleep deprivation, induced by ＂flower pot＂ technique, on spatial reference memory and working memory require further research. OBJECTIVE： To observe the effect of progressive paradoxical sleep deprivation in rats, subsequent to learning, on memory using the Morris Water Maze. DESIGN, TIME AND SETTING： Controlled observation experiment. The experiment was performed at the Laboratory of Neurobiology, Department of Anatomy, Histology and Embryology, School of Basic Medical Sciences, Lanzhou University from December 2006 to October 2007. MATERIALS： Twenty-eight, male, Wistar rats, 3-4 months old, were provided by the Experimental Animal Center of Lanzhou University. The Morris Water Maze and behavioral analyses system was purchased from Genheart Company, Beijing, China. METHODS： All animals, according to a random digits table, were randomly divided into paradoxical sleep deprivation, tank control, and home cage control groups. Paradoxical sleep deprivation was induced by the ＂flower pot＂ technique for 72 hours, housing the rats on small platforms over water. Rats in the ＂tank control＂ and ＂home cage control＂ groups were housed either in a tank with large platforms over the water or in normal cages without paradoxical sleep deprivation. MAIN OUTCOME MEASURES： Morris Water Maze was employed for task learning and spatial memory testing. Rats in all groups were placed at six random starting points each day for four consecutive days. Each placement was repeated for two trials; the first trial represented reference memory and the second working memory. Rats in the first trial were allowed to locate the submerged platform within 120 seconds. Data, including swimming distance, escape latency, swimming velocity, percentage of time in correct quarter, and memory scores were recorded and analyzed automatically by behavioral analyses systems for Morris Water Maze. RESULTS： Twenty-eight rats were included in the final analysis, without any loss. In the first trial, between day 2 and 4, escape latency and swimming distance increased significantly in the paradoxical sleep deprivation group compared to the home cage control and tank control groups （P 〈 0.01）; percentage of time in correct quarter and memory scores, however, decreased in the paradoxical sleep deprivation group compared to the home cage control and tank control groups （P 〈 0.01）. The escape latency, swimming distance, percentage of time in correct quarter, and memory scores in the second trial was not significantly different among the three groups （P 〉 0.05）. CONCLUSION： Paradoxical sleep deprivation inhibits spatial reference memory, but not working memory.

Maternal sleep deprivation induces gut microbial dysbiosis and neuroinflammation in offspring rats

Maternal sleep deprivation(MSD)is a global public health problem that affects the physical and mental development of pregnant women and their newborns.The latest research suggests that sleep deprivation(SD)disrupts the gut microbiota,leading to neuroinflammation and psychological disturbances.However,it is unclear whether MSD affects the establishment of gut microbiota and neuroinflammation in the newborns.In the present study,MSD was performed on pregnant SpragueDawley rats in the third trimester of pregnancy(gestational days 15-21),after which intestinal contents and brain tissues were collected from offspring at different postnatal days(P1,P7,P14,and P56).Based on microbial profiling,microbial diversity and richness increased in pregnant rats subjected to MSD,as reflected by the significant increase in the phylum Firmicutes.In addition,microbial dysbiosis marked by abundant Firmicutes bacteria was observed in the MSD offspring.Furthermore,quantitative real-time polymerase chain reaction(q RT-PCR)and enzyme-linked immunosorbent assay(ELISA)showed that the expression levels of proinflammatory cytokines interleukin 1β(IL-1β)and tumor necrosis factorα(TNF-α)were significantly higher in the MSD offspring at adulthood(P56)than in the control group.Through Spearman correlation analysis,IL-1βand TNF-αwere also shown to be positively correlated with Ruminococcus_1 and Ruminococcaceae_UCG-005 at P56,which may determine the microbiota-host interactions in MSDrelated neuroinflammation.Collectively,these results indicate that MSD changes maternal gut microbiota and affects the establishment of neonatal gut microbiota,leading to neuroinflammation in MSD offspring.Therefore,understanding the role of gut microbiota during physiological development may provide potential interventions for cognitive dysfunction in MSD-impacted offspring.

Effects of sleep deprivation on cognitive functions

Sleep deprivation （SD） is a common condition that afflicts many people in modem life. Deficits in daytime perfor- mance due to SD are experienced universally. Recent evidence indicates that SD causes impairments in cognitive functions. However, the mechanisms that SD impairs cognitive functions are not clear. This review will focus on the behavioral and neural effects of SD with the aim to elucidate the possible mechanisms of SD-induced deterioration in cognitive functions and to identify directions for future research.

G-protein coupled receptors and synaptic plasticity in sleep deprivation

Insufficient sleep has been correlated to many physiological and psychoneurological disorders.Over the years,our understanding of the state of sleep has transcended from an inactive period of rest to a more active state involving important cellular and molecular processes.In addition,during sleep,electrophysiological changes also occur in pathways in specific regions of the mammalian central nervous system(CNS).Activity mediated synaptic plasticity in the CNS can lead to long-term and sometimes permanent strengthening and/or weakening synaptic strength affecting neuronal network behaviour.Memory consolidation and learning that take place during sleep cycles,can be affected by changes in synaptic plasticity during sleep disturbances.G-protein coupled receptors(GPCRs),with their versatile structural and functional attributes,can regulate synaptic plasticity in CNS and hence,may be potentially affected in sleep deprived conditions.In this review,we aim to discuss important functional changes that can take place in the CNS during sleep and sleep deprivation and how changes in GPCRs can lead to potential problems with therapeutics with pharmacological interventions.

Behavioral study of sleep deprivation model in caffeine and light induced zebrafish

Objective:To compare the differences in behavior of sleep deprivation models in caffeine and light induced zebrafish.Methods:A total of 72 zebrafish larvae,were selected 5 d after fertilization and randomly divided into blank control group,caffeine and light group,with 24 larvae in each group.The blank control group was given normal breeding for 24 h,while on the basis of treatment in the blank control group,the caffeine group was exposed to 200μmol/L caffeine in water and the light group to 200 lux light conditions continuously for 24 h.Results:The pigmentation of zebrafish head in the light group and the caffeine group was slightly shallow with edema of yolk sac.The activity time of the light group and the caffeine group increased compared with the blank control group(P<0.01,P<0.05),but there was no significiant difference in activity time between the light group and the caffeine group(P>0.05),The small movement time of the light group was significantly more than the caffeine group(P<0.01),while the medium movement time of the caffeine group was more than light group(P<0.05).Conclusion:Both light and caffeine can induce zebrafish sleep deprivation model effectively,and have effects on zebrafish phenotype to a certain degree,but there are differences in motor form between the two kinds of sleep-deprivation models.

The Role of Sleep Deprivation in Arrhythmias

Sleep is essential to the normal psychological and physiological activities of the human body.Increasing evidence indicates that sleep deprivation is associated with the occurrence,development,and poor treatment effects of various arrhythmias.Sleep deprivation affects not only the peripheral nervous system but also the central nervous system,which regulates the occurrence of arrhythmias.In addition,sleep deprivation is associated with apoptotic pathways,mitochondrial energy metabolism disorders,and immune system dysfunction.Although studies increasingly suggest that pathological sleep patterns are associated with various atrial and ventricular arrhythmias,further research is needed to identify specific mechanisms and recommend therapeutic interventions.This review summarizes the findings of sleep deprivation in animal experiments and clinical studies,current challenges,and future research directions in the field of arrhythmias.

Effect of chronic sleep deprivation on peak bone mass in rats: An experimental study

Objective:To investigate the effects of chronic sleep deprivation(CSD)on bone microstructure and peak bone mass(PBM)in SD rats.Methods:Twenty-four SD rats were randomly divided into CSD group and control group.In the CSD group,a CSD model was established using a new sleep deprivation instrument for rats and mice,and intervened for 5 weeks.Bone turnover markers including P1NP and CTX-1 before and after the experiment were observed.After the experiment,the left femur were scanned by Micro-CT,and the cortical bone and bone trabecula were three-dimensionally reconstructed,respectively.The bone mineral density(BMD)and relevant parameters were detected.Results:CT images of the femur(proximal ends)showed significant trabecular loss in CSD rats.Trabecular parameters including bone volume fraction(BV/TV),trabecular number(Tb.N)and trabecular separation(Tb.Sp)in the CSD group were all lower than those in the control group.The bone cortex of the middle segment of the femur and tibia in CSD rats was also lower than that in the control group.The parameters of bone cortex including total tissue area(Tt.Ar),cortical bone area(Ct.Ar)and cortical bone thickness(Ct.Th)in the CSD group were significantly lower than those in the control group(P<0.01).After chronic CSD,BMD of both bone trabecula and bone cortex of the femur was lower,while the corresponding P1NP and CTX-1 were significantly higher than those in the control group.Conclusion:Sleep plays an important role in PBM formation.CSD accelerates bone turnover and thus significantly reducing PBM in SD rats.

Sleep deprivation and associated factors among students of the Institute of Health in Jimma University, Southwest Ethiopia

Objective:Despite getting sufficient sleep being one of the most important things that we can do to keep our body and mind healthy,sleep deprivation has become a major public health concern.This study aimed to determine the prevalence of sleep deprivation and its associated factors among students of the Institute of Health in Jimma University.Methods:An institution-based cross-sectional study was conducted from April 10 to April 24 in 2019.Data were collected from 365 randomly selected participants and analyzed using Statistical Package for the Social Sciences(SPSS;version 23).Multivariate logistic regression analysis was used to identify the factors associated with sleep deprivation.The level of significance was declared at a P-value of<0.05.Results:A total of 365 participants participated,with a response rate of 97.6%.The study findings showed that 60.8%of students had sleep deprivation and 68.2%had sleep latency.Health problems(adjusted odds ratio[AOR]=1.91[95%confidence interval{CI}=1.01–3.58]),alcohol consumption[AOR=0.42(95%CI=0.2–0.89)],cigarette smoking[AOR=0.31(95%CI=0.09–0.93)],khat chewing[AOR=0.47(95%CI=0.12–0.82)],use of an electronic device before bedtime[AOR=5.26(95%CI=1.78–15.52)],and cumulative grade point average(CGPA)[AOR=0.48(95%CI=0.27–0.83)]were significantly associated with sleep deprivation.Conclusions:Sleep deprivation was common in the study area.This is mainly due to health problems,substance utilization,long-time use of an electronic device,and low CGPA.Therefore,a strategy and system should be established to limit substance use,enhance proper use of electronic devices,and create awareness on the impact of nonoptimal sleep.

Correlation between interaction anxiousness and sleep deprivation among undergraduate students

Sleep deprivation is a common problem among university students,it causes lowered cognitive skills,higher tend of suicide,risk-taking behavior and interaction anxiety.By using the Pittsburgh sleep quality index(PSQI)and Interaction Anxiousness Scale(IAS),the survey on the sleep quality and interaction anxiousness was carried out among 124 undergraduate students,in order to found the correlation between sleep deprivation and interaction anxiousness.The results showed a strong positive correlation between them.This study also investigates the difference of PSQI and IAS among students with varied disciplines and grades,and findings illustrated a poor sleep quality as well as poor interpersonal communication situation among university students.

Sleep Deprivation Selectively Down-Regulates Astrocytic 5-HT2B Receptors and Triggers Depressive-Like Behaviors via Stimulating P2X7 Receptors in Mice

Chronic loss of sleep damages health and disturbs the quality of life.Long-lasting sleep deprivation(SD)as well as sleep abnormalities are substantial risk factors for major depressive disorder,although the underlying mechanisms are not clear.Here,we showed that chronic SD in mice promotes a gradual elevation of extracellular ATP,which activates astroglial P2X7 receptors(P2X7Rs).Activated P2X7Rs,in turn,selectively down-regulated the expression of 5-HT2B receptors(5-HT2BRs)in astrocytes.Stimulation of P2X7Rs induced by SD selectively suppressed the phosphorylation of AKT and FoxO3 a in astrocytes,but not in neurons.The overexpression of FoxO3a in astrocytes inhibited the expression of 5-HT2BRs.Down-regulation of 5-HT2BsRs instigated by SD suppressed the activation of STAT3 and relieved the inhibition of Ca2+-dependent phospholipase A2.This latter cascade promoted the release of arachidonic acid and prostaglandin E2.The depression-like behaviors induced by SD were alleviated in P2X7R-KO mice.Our study reveals the mechanism underlying chronic SD-induced depression-like behaviors and suggests 5-HT2BRs as a key target for exploring therapeutic strategies aimed at the depression evoked by sleep disorders.

Effects of sleep deprivation on polysomnography and executive function in patients with depression

Anumber of therapies have been developed in the past decades.About two thirds of patients can be seizure free with antiepileptic drugs.1 Other patients are drug resistant,some of whom are good candidates for epileptic focus resection and become seizure free after surgery.2 The treatment for drug-resistant patients who are not eligible for resection is still challenging.Traditionally,these patients can receive palliative surgery such as callosotomy and multiple subpial transection,3,4 but the long-term outcomes of these procedures are not satisfactory.5-7 In the past decades,neuromodulation techniques have been applied in the treatment of epilepsy.Much evidence has been accumulated about the therapeutic effects of vagus nerve stimulation for epilepsy.In contrast to peripheral nerve stimulation,brain stimulation techniques have also been developed for patients with epilepsy recently.

Sleep deprivation reorganizes the dynamic configurations of default mode network activity during recovery sleep

Sleep deprivation causes disturbances of the neural activity, leading to the impairment of brain functions. However, the exact mechanism of sleep deprivation and how it affects the dynamics of brain activity during the recovery sleep remains unclear. In the current study, we performed sleep deprivation experiments on ten adult rats, and recorded the local field potentials from default mode network(DMN) regions during sleep before and after sleep deprivation. The DMN dynamics was assessed with the configurations of coactive micropatterns(CAMPs) using our previously proposed CAMP method. Our analysis revealed that the effects of sleep deprivation on DMN dynamics in the slow-wave sleep(SWS) state and the rapid eye-movement sleep(REM)state were disparate. Dynamic configurations of DMN activity in the SWS state were significantly impaired after sleep deprivation, with increased occurrence of low-activity CAMP and reorganized transition structure across three CAMPs. Moreover,enhanced functional connectivity and improved efficiencies in all CAMP networks were observed during the SWS state in the recovery sleep. However, there were no significant alterations in either DMN dynamics or CAMP network structures in the REM sleep state after sleep deprivation. Our results described the alterations of DMN dynamics in different sleep states after sleep deprivation, and illustrated the differential effects of sleep deprivation on two sleep states. These findings demonstrated the underlying neural mechanisms of the effects of sleep deprivation on DMN activity during sleep and increased our understanding of the physiological roles of the DMN in maintain sleep homeostasis after sleep deprivation.

Preoperative Acute Sleep Deprivation Causes Postoperative Pain Hypersensitivity and Abnormal Cerebral Function

Preoperative sleep loss can amplify post-operative mechanical hyperalgesia.However,the underlying mechanisms are still largely unknown.In the current study,rats were randomly allocated to a control group and an acute sleep deprivation(ASD)group which experienced 6 h ASD before surgery.Then the variations in cerebral function and activity were investigated with multi-modal techniques,such as nuclear magnetic resonance,functional magnetic resonance imaging,c-Fos immunofluorescence,and electrophysiology.The results indicated that ASD induced hyperalgesia,and the metabolic kinetics were remarkably decreased in the striatum and midbrain.The functional connectivity(FC)between the nucleus accumbens(NAc,a subregion of the ventral striatum)and the ventrolateral periaqueductal gray(vLPAG)was significantly reduced,and the c-Fos expression in the NAc and the vLPAG was suppressed.Furthermore,the electrophysiological recordings demonstrated that both the neuronal activity in the NAc and the vLPAG,and the coherence of the NAc-vLPAG were suppressed in both resting and task states.This study showed that neuronal activity in the NAc and the vLPAG were weakened and the FC between the NAc and the vLPAG was also suppressed in rats with ASD-induced hyperalgesia.This study highlights the importance of preoperative sleep management for surgical patients.

Effects of modafinil on vestibular function during 24 hour sleep deprivation

The aim of this research was to investigate the effects of modafinil,a new wake-promoting agent,on vestibular function during 24 h sleep deprivation(SD)so as to provide experimental evidence for the rational use of this drug among air crew.Eight young,healthy male volunteers were exposed to two 24 h periods of continuous wakefulness during the crossover experiment.Initially,200 mg dose of modafinil was given,and one week later,a matching placebo was administered.The SD time started from 08:00 of the first day to 08:00 of the second day.Drugs were given at 0:00 on the second day.Vestibular function was tested at 21:00 on the first day and 1,3,5,7 h after drug administration.The accuracy of saccade tracking and gains in visual-vestibular optokinetic reflex(VVOR)and optokinetic nystagmus(OKN)in the placebo group decreased during 24 h SD,especially at 01:00–05:00 on the second day,while OKN gains in the modafinil group increased significantly.There were no significant differences in the other vestibular functional indices between the modafinil group and placebo group.The 24 h SD can influence vestibular function to a certain degree,but modafinil may improve OKN.

CX3C-chemokine receptor 1 modulates cognitive dysfunction induced by sleep deprivation

Background:Microglia plays an indispensable role in the pathological process of sleep deprivation(SD).Here,the potential role of microglial CX3C-chemokine receptor 1(CX3CR1)in modulating the cognition decline during SD was evaluated in terms of microglial neuroinflammation and synaptic pruning.In this study,we aimed to investigat whether the interference in the microglial function by the CX3CR1 knockout affects the CNS's response to SD.Methods:Middle-aged wild-type(WT)C57BL/6 and CX3CR1^(−/−)mice were either subjected to SD or allowed normal sleep(S)for 8 h to mimic the pathophysiological changes of middle-aged people after staying up all night.After which,behavioral and histological tests were used to explore their different changes.Results:CX3CR1 deficiency prevented SD-induced cognitive impairments,unlike WT groups.Compared with the CX3CR1^(−/−)S group,the CX3CR1^(−/−)SD mice reported a markedly decreased microglia and cellular oncogene fos density in the dentate gyrus(DG),decreased expression of pro-inflammatory cytokines,and decreased microglial phagocytosis-related factors,whereas increased levels of anti-inflammatory cytokines in the hippocampus and a significant increase in the density of spines of the DG were also noted.Conclusions:These findings suggest that CX3CR1 deficiency leads to different cerebral behaviors and responses to SD.The inflammation-attenuating activity and the related modification of synaptic pruning are possible mechanism candidates,which indicate CX3CR1 as a candidate therapeutic target for the prevention of the sleep loss-induced cognitive impairments.

Sleep during and following critical illness:A narrative review

Sleep is a complex process influenced by biological and environmental factors.Disturbances of sleep quantity and quality occur frequently in the critically ill and remain prevalent in survivors for at least 12 mo.Sleep disturbances are associated with adverse outcomes across multiple organ systems but are most strongly linked to delirium and cognitive impairment.This review will outline the predisposing and precipitating factors for sleep disturbance,categorised into patient,environmental and treatment-related factors.The objective and subjective methodologies used to quantify sleep during critical illness will be reviewed.While polysomnography remains the gold-standard,its use in the critical care setting still presents many barriers.Other methodologies are needed to better understand the pathophysiology,epidemiology and treatment of sleep disturbance in this population.Subjective outcome measures,including the Richards-Campbell Sleep Questionnaire,are still required for trials involving a greater number of patients and provide valuable insight into patients’experiences of disturbed sleep.Finally,sleep optimisation strategies are reviewed,including intervention bundles,ambient noise and light reduction,quiet time,and the use of ear plugs and eye masks.While drugs to improve sleep are frequently prescribed to patients in the ICU,evidence supporting their effectiveness is lacking.

Role of Cannabinoid CB1 Receptor in Object Recognition Memory Impairment in Chronically Rapid Eye Movement Sleep-deprived Rats

Objective We aimed to investigate whether antagonism of the cannabinoid CB1 receptor(CB1R)could affect novel object recognition(NOR)memory in chronically rapid eye movement sleep-deprived(RSD)rats.Methods The animals were examined for recognition memory following a 7-day chronic partial RSD paradigm using the multiple platform technique.The CB1R antagonist rimonabant(1 or 3 mg/kg,i.p.)was administered either at one hour prior to the sample phase for acquisition,or immediately after the sample phase for consolidation,or at one hour before the test phase for retrieval of NOR memory.For the reconsolidation task,rimonabant was administered immediately after the second sample phase.Results The RSD episode impaired acquisition,consolidation,and retrieval,but it did not affect the reconsolidation of NOR memory.Rimonabant administration did not affect acquisition,consolidation,and reconsolidation;however,it attenuated impairment of the retrieval of NOR memory induced by chronic RSD.Conclusions These findings,along with our previous report,would seem to suggest that RSD may affect different phases of recognition memory based on its duration.Importantly,it seems that the CB1R may,at least in part,be involved in the adverse effects of chronic RSD on the retrieval,but not in the acquisition,consolidation,and reconsolidation,of NOR memory.