REM Sleep Deprivation Research Articles

Neurogenesis in the rat neonate's hippocampus with maternal short-term REM sleep deprivation restores by royal jelly treatment.

BackgroundNumerous studies have shown the effects of rapid eye movement sleep deprivation (REM‐SD) on behavior and brain structures. The impact of REM‐SD on learning and memory, thus neurogenesis, has been reported in previous studies. Royal jelly (RJ) is known as the wealthiest biological nutrient with various physiological properties. This study aimed to study the possible effect of RJ on neurogenesis of the rat hippocampus neonates following exposure of mother to REM‐SD during pregnancy.MethodsThirty neonate rats from 15 pregnant Wistar rats were used. To induce REM‐SD, the flowerpot method was used. The pregnant rats were divided into five groups (n = 3): group 1, no treatment; group 2, REM‐SD; groups 3, 4, and 5, REM‐SD +RJ. The former group received 72 h REM‐SD during pregnancy (days 7, 14, 21), and the latter group received REM‐SD + RJ (three trial groups). At week 4, the rat neonates of all groups were sacrificed (n = 6 each group). Their brains were fixed, removed, and prepared for Nissl and Hoechst 33342 staining. By using real time polymerase chain reaction methode the brain‐derived neurotrophic factor BDNF gene expression was studied (RT‐PCR), brain‐derived neurotrophic factor (BDNF) gene expression was studied. The results were analyzed statistically, and the Pv < .05 was considered significant.ResultsThe results showed a significant decrease in the number of neurons in the hippocampus of neonatal rats of REM‐SD mothers compared to the neonates of the mother with REM‐SD + RJ. REM‐SD also led to an increase in apoptosis reaching the neonates from the REM‐SD + RJ animals. High expression of BDNF was observed in the hippocampus of the neonates from REM‐SD + RJ treated mothers.ConclusionRJ acts as a neuroprotective agent that could compensate for the effects of REM‐SD on learning and memory via restoring neurogenesis.

Effect of the cPKCγ-Ng Signaling System on Rapid Eye Movement Sleep Deprivation-Induced Learning and Memory Impairment in Rats.

Objective: Rapid eye movement sleep deprivation (REM-SD) can cause a decline in learning and memory and lead to changes in behavior. Therefore, REM sleep plays a key role in processes that govern learning and memory. However, the mechanism underlying REM-SD-induced learning and memory impairment is unclear and the underlying molecular signaling still needs to be identified. In the present study, we investigated the role of the cPKCγ-Ng signaling pathway in REM-SD-induced learning and memory impairment.Method: Sixty male rats were divided into Control, REM-SD, REM-SD+cPKCγ activator PMA, REM-SD+cPKCγ inhibitor H-7, and sleep revival (SR) groups. The Morris water maze was used to assess spatial learning and memory. Western blot analysis was used to detect cPKCγ total protein expression and membrane translocation levels, and Ng total protein expression and phosphorylation levels.Results: The REM-SD group performed worse on the Morris water maze test than the control group. Western blot analysis showed that cPKCγ membrane translocation and Ng phosphorylation levels were significantly lower in the REM-SD group. SR following REM-SD restored learning and memory ability, cPKCγ transmembrane translocation, and Ng phosphorylation levels, but not to levels observed before REM-SD. PMA and H-7 significantly improved/disrupted task ability as well as cPKCγ transmembrane translocation and Ng phosphorylation levels in REM-SD rats.Conclusion: The REM-SD induced learning and memory impairment in rats and may be associated with the cPKCγ-Ng signaling pathway. Specifically, activation of the cPKCγ-Ng signaling pathway may protect against REM-SD.

Effects of sleep deprivation of various durations on novelty-related object recognition memory and object location memory in mice

Sleep is essential for important physiological functions. Impairment of learning and memory function caused by lack of sleep is a common physiological phenomenon of which underlying changes in synaptic plasticity in the hippocampus are not well understood. The possible different effects of sleep deprivation (SD) lasting for various durations on learning and memory function and hippocampal synaptic plasticity are still not completely clear. In this study, we used a modified multiple platform method (MMPM) to induce rapid eye movement SD (REM SD), lasting for 24 h, 48 h, and 72 h, separately. The novel place recognition (NPR) and novel object recognition (NOR) tasks were used to test the novelty-related object recognition memory (ORM) and object location memory (OLM) of mice. Then, hippocampal synaptic plasticity was evaluated after all behavioural experiments. The results showed that REM SD played a key role in OLM but not in ORM. Specifically, 24 h REM SD improved novelty-related OLM, accompanied by a significantly increased hippocampal synaptic plasticity, including gain of dendritic spines, increased expression of hippocampal GluA1, and enhanced long-term potentiation (LTP), whereas 48 h REM SD showed no effect on OLM or the hippocampal synaptic plasticity mentioned above; however, 72 h REM SD impaired novelty-related OLM and weakened hippocampal synaptic plasticity, including serious loss of dendritic spines, decreased expression of hippocampal GluA1, and significantly attenuated LTP. Our results suggest that REM SD of various durations has different effects on both novelty-related OLM and hippocampal synaptic plasticity.

Evaluation of Pain Tolerance Threshold Following Administration of Anti-TNF-α in REM Sleep-deprived Male Wistar Rats

Background and Aim: The level of Tumor Necrosis Factor-alpha (TNF-α) changes by Rapid Eye Movement (REM) sleep deprivation. TNF-α is a known biomarker of REM Sleep Deprivation (RSD). Prior studies have shown that any alteration in REM sleep can increase the amount of TNF-α. Accordingly, the Pain Tolerance Threshold (PTT) is believed to be increased in patients with insomnia after using anti-TNF-α or Infliximab (IFX). The present study aims to demonstrate the effect of IFX and its importance in the pain management of hospital inpatients. Methods and Materials/Patients: Seventy-two male Wistar rats in 9 groups were studied after obtaining the approval of the ethics committee of Tehran University of Medical Sciences (CNS. Protocol-ICSS-940816). Remicade was used for inducing the anti-TNF-α. Multiple platform water-tank was used for REM sleep deprivation induction. Pain tolerance was measured on a hot plate apparatus. Results: There was a significant increase in the duration of the rats’ tolerance on the hot plate between the saline group and the group that received IFX (0.2 mg/kg) (F2=8.363) (P&lt;0.001). Conclusion: Chronic SD can cause neuronal damage due to neuroinflammatory insults. REM sleep deprivation, in the long run, sensitizes the brain to neurodegenerative insults via the inflammatory mechanism, to some extent through the TNFα-associated pathways.

Correction to: REM Sleep Deprivation Impairs Learning and Memory by Decreasing Brain O-GlcNAc Cycling in Mouse

Correction to: REM Sleep Deprivation Impairs Learning and Memory by Decreasing Brain O-GlcNAc Cycling in Mouse

Lactobacillus fermentum PS150 promotes non-rapid eye movement sleep in the first night effect of mice

The first night effect (FNE) is a type of sleep disturbance caused by an unfamiliar environment, which leads to difficulty falling asleep and reduced sleep duration. Previously, we reported that Lactobacillus fermentum PS150 (PS150) improves sleep conditions in a pentobarbital-induced sleep mouse model. In this study, we aimed to evaluate the effect of PS150 on the FNE in mice. Briefly, mice were implanted with electrodes and orally administered PS150 for four weeks, and then the FNE was induced by cage changing. Analysis of polysomnographic signals revealed that intervention with PS150 restored non-rapid eye movement (NREM) sleep length under the FNE. Compared to diphenhydramine, a commonly used sleep aid, PS150 had no unwanted side effects, such as rapid eye movement (REM) sleep deprivation and fragmented sleep. Moreover, temporal analysis revealed that PS150 efficiently reduced both sleep latency and time spent restoring normal levels of REM sleep. Taken together, these results suggest that PS150 efficiently ameliorates sleep disturbance caused by the FNE. Additionally, V3–V4 16S rRNA sequencing revealed significant increases in Erysipelotrichia, Actinobacteria, and Coriobacteriia in fecal specimens of the PS150-treated group, indicating that PS150 induces gut microbiota remodeling.

Cerebral capillary blood flow upsurge during REM sleep is mediated by A2a receptors.

Sleep is generally viewed as a period of recovery, but how the supply of cerebral blood flow (CBF) changes across sleep/wake states has remained unclear. Here, we directly observe red blood cells (RBCs) within capillaries, where the actual substance exchange between the blood and neurons/glia occurs, by two-photon microscopy. Across multiple cortical areas, average capillary CBF is largely increased during rapid eye movement (REM) sleep, whereas it does not differ between periods of active wakefulness and non-REM sleep. Capillary RBC flow during REM sleep is further elevated following REM sleep deprivation, suggesting that capillary CBF reflects REM sleep pressure. At the molecular level, signaling via adenosine A2a receptors is crucial; in A2a-KO mice, capillary CBF upsurge during REM sleep is dampened, and effects of REM sleep pressure are abolished. These results provide evidence regarding the dynamics of capillary CBF across sleep/wake states and insights to the underlying mechanisms.

REM Sleep Deprivation Impairs Learning and Memory by Decreasing Brain O-GlcNAc Cycling in Mouse.

Rapid eye movement (REM) sleep is implicated learning and memory (L/M) functions and hippocampal long-term potentiation (LTP). Here, we demonstrate that REM sleep deprivation (REMSD)-induced impairment of contextual fear memory in mouse is linked to a reduction in hexosamine biosynthetic pathway (HBP)/O-GlcNAc flux in mouse brain. In mice exposed to REMSD, O-GlcNAcylation, and O-GlcNAc transferase (OGT) were downregulated while O-GlcNAcase was upregulated compared to control mouse brain. Foot shock fear conditioning (FC) induced activation of protein kinase A (PKA) and cAMP response element binding protein (CREB), which were significantly inhibited in brains of the REMSD group. Intriguingly, REMSD-induced defects in L/M functions and FC-induced PKA/CREB activation were restored upon increasing O-GlcNAc cycling with glucosamine (GlcN) or Thiamet G. Furthermore, Thiamet G restored the REMSD-induced decrease in dendritic spine density. Suppression of O-GlcNAcylation by the glutamine fructose-6-phosphate amidotransferase (GFAT) inhibitor, 6-diazo-5-oxo-L-norleucine (DON), or OGT inhibitor, OSMI-1, impaired memory function, and inhibited FC-induced PKA/CREB activation. DON additionally reduced the amplitude of baseline field excitatory postsynaptic potential (fEPSP) and magnitude of long-term potentiation (LTP) in normal mouse hippocampal slices. To our knowledge, this is the first study to provide comprehensive evidence of dynamic O-GlcNAcylation changes during the L/M process in mice and defects in this pathway in the brain of REM sleep-deprived mice. Our collective results highlight HBP/O-GlcNAc cycling as a novel molecular link between sleep and cognitive function.

Rapid Eye Movement Sleep Deprivation Combined With Fluoxetine Protects Against Depression-Induced Damage and Apoptosis in Rat Hippocampi via A1 Adenosine Receptor.

Background: Rapid eye movement sleep deprivation (REMSD) and fluoxetine affect depression, yet the detailed molecular mechanisms were not clear.Methods: Rat depression chronic unpredictable stress was constructed, and the body weight of rats was measured. The efficacy of REMSD and fluoxetine on the pleasure experience, exploration, and cognition of rats with depression was determined by the Sucrose preference test, the open field test, and Morris water task, respectively. The effects of REMSD and fluoxetine on depression-induced damage and apoptosis in rat hippocampi were detected using hematoxylin–eosin staining and terminal transferase-mediated biotin 2′-deoxyuridine, 5′-triphosphate nick end labeling. A1 adenosine receptor content was measured by immunohistochemistry. Relative expressions of the A1 adenosine receptor, proteins related to apoptosis (B Bcl-2-associated X protein; B-cell lymphoma 2), phosphoinositide 3-kinase, P38 mitogen-activated protein kinase, cFos, and adenosine deaminase RNA specific two were quantified by quantitative real-time polymerase chain reaction and Western blot as needed.Results: Depression decreased rat weight. REMSD combined with fluoxetine increased body weight, prompted rat behavior, alleviated depression-induced damage, attenuated apoptosis, and promoted A1 adenosine receptor level in rat hippocampi. Furthermore, the combined therapy upregulated expressions of A1 adenosine receptor, B-cell lymphoma 2, and phosphoinositide 3-kinase but downregulated those of B-cell lymphoma 2-associated X protein, P38 mitogen-activated protein kinase, cFos, and adenosine deaminase RNA specific 2 in the hippocampi of rats with depression.Conclusion:REMSD combined with fluoxetine protected rats against depression-induced damage and apoptosis in the hippocampus via the A1 adenosine receptor, providing a possible treatment strategy for depression.

The effects of glucagon-like peptide 1 receptor agonist (exenatide) on memory impairment, and anxiety- and depression-like behavior induced by REM sleep deprivation

Previous investigations have shown that REM sleep deprivation impairs the hippocampus‐dependent memory, long-term potentiation and causing mood changes. The aim of the present study was to explore the effects of exenatide on memory performance, anxiety- and depression like behavior, oxidative stress markers, and synaptic protein levels in REM sleep deprived rats.A total of 40 male Wistar rats were randomly divided to control, exenatide-treated control, sleep deprivation (SD), wide platform (WP) and exenatide-treated SD groups. During experiments, exenatide treatment (0.5 μg/kg, subcutaneously) was applied daily in a single dose for 9 days. Modified multiple platform method was employed to generate REM sleep deprivation for 72 h. The Morris water maze test was used to assess memory performance. Anxiety- and depression-like behaviors were evaluated by open field test (OFT), elevated plus maze (EPM) forced swimming test (FST), respectively 72 h after REMSD. The levels of Ca2+/calmodulin-dependent protein kinase II (CaMKII) and postsynaptic density proteins 95 (PSD95) were measured in tissues of hippocampus and prefrontal cortex. The content of malondialdehyde (MDA) and reduced glutathione (GSH) were also measured.In the present study, an impairment in memory was observed in SD rats at the 24th hour of SD in compare to those of other groups. REMSD increased depression-like behavior in FST as well as the number of rearing and crossing square in OFT. Anxiety is the most common comorbid condition with depressive disorders. Contents of CaMKII and PSD95 decreased in hippocampus of SD rats. Exenatide treatment improved the impaired memory of SD rats and increased CaMKII content in hippocampus There was no difference in MDA and GSH levels among groups. Exenatide treatment also diminished locomotor activity in OFT.In conclusion, treatment with exenatide, at least in part, prevented from these cognitive and behavioral changes possibly through normalizing CaMKII levels in the hippocampus.

Rapid eye movement sleep deprivation impairs neuronal plasticity and reduces hippocampal neuronal arborization in male albino rats: Noradrenaline is involved in the process.

Rapid eye movement sleep (REMS) favors brain development and memory, while it is decreased in neurodegenerative diseases. REMS deprivation (REMSD) affects several physiological processes including memory consolidation; however, its detailed mechanism(s) of action was unknown. REMS reduces, while REMSD elevates noradrenaline (NA) level in the brain; the latter induces several deficiencies and disorders, including changes in neuronal cytomorphology and apoptosis. Therefore, we proposed that REMS- and REMSD-associated modulation of NA level might affect neuronal plasticity and affect brain functions. Male albino rats were REMS deprived by flower-pot method for 6days, and its effects were compared with home cage and large platform controls as well as post-REMSD recovered and REMS-deprived prazosin (α1-adrenoceptor antagonist)-treated rats. We observed that REMSD reduced CA1 and CA3 neuronal dendritic length, branching, arborization, and spine density, while length of active zone and expressions of pre- as well as post-synaptic proteins were increased as compared to controls; interestingly, prazosin prevented most of the effects in vivo. Studies on primary culture of neurons from chick embryo brain confirmed that NA at lower concentration(s) induced neuronal branching and arborization, while higher doses were destructive. The findings support our contention that REMSD adversely affects neuronal plasticity, branching, and synaptic scaffold, which explain the underlying cytoarchitectural basis of REMSD-associated patho-physio-behavioral changes. Consolidation of findings of this study along with that of our previous reports suggest that the neuronal disintegration could be due to either withdrawal of direct protective and proliferative role of low dose of NA or indirect effect of high dose of NA or both.

Alteration of fear behaviors in sleep-deprived adolescent rats: increased fear expression and delayed fear extinction

ABSTRACT Disruption of sleep due to acute or chronic stress can lead to changes in emotional memory processing. Sleep disturbances are highly prevalent in post-traumatic stress disorder (PTSD), but still, the contribution of sleep deprivation on the susceptibility to PTSD has received little attention. To determine whether rapid eye movement sleep deprivation (SD) alters the development of fear expression or fear-associated memory impairment in adolescent rats, we performed animal emotional behavior tests using an SD animal model with the flowerpot technique. SD rats showed an increase in locomotor activity frequency and a decrease in sucrose consumption compared to control rats. An increase in freezing behavior during shock trials was observed in SD rats. Noticeably, it was observed that when applying the SD condition after fear stimuli exposure, fear extinction was delayed more in SD rats than in control rats. Overall, these results indicate that SD in adolescent rats leads to increased locomotor activity and anhedonic behavior, as well as increased fear expression and delayed fear extinction, suggesting that SD would lead to increased severity of PTSD-like phenotype.

Electrophysiological and neurochemical evaluation of the adverse effects of REM sleep deprivation and epileptic seizures on rat's brain

AimThe current study aims to investigate the impact of paradoxical (REM) sleep deprivation and/or epileptic seizures on rat's cortical brain tissues. Main methodsAnimals were divided into four groups; control, epileptic, REM sleep deprived and epileptic subjected to REM sleep deprivation. Electrocorticogram (ECoG) signals were recorded and quantitatively analyzed for each group. Concentrations of amino acid neurotransmitters; proinflammatory cytokines; and oxidative stress parameters; and acetylcholinesterase activity were determined in the cortex of the animals in different groups. Key findingsResults showed significant variations in the spectral distribution of ECoG waves in the epilepsy model, 24- and 48-hours of REM sleep deprivation and their combined effects indicating a state of cortical hyperexcitability. Significant increases in NO and taurine and significant decrement in glutamine, GABA and glycine were determined. In REM sleep deprived rats significant elevation in glutamate, aspartate, glycine and taurine and a significant lowering in GABA were obtained. This was accompanied by significant reduction in AchE and IL-β. In the cortical tissue of epileptic rats deprived from REM sleep significant increases in lipid peroxidation, TNF-α, IL-1β, IL-6 and aspartate and a significant reduction in AchE were observed. SignificanceThe present data indicate that REM sleep deprivation induces an increase in lipid peroxidation and storming in proinflammatory cytokines in the cortex of rat model of epilepsy during SRS. These changes are associated with a decreased seizure threshold as inferred from the increase in alpha and Beta waves and a decrease in Delta waves of ECoG.

Intermittent REM sleep deprivation attenuates the development of morphine tolerance and dependence in male rats

Opioid agonists are used in clinic for pain management, however this application is challenged by development of tolerance and dependence following prolonged exposure. Various approaches have been suggested to address this concern, however, there is still no consensus among the researchers. Neural processing of sleep and nociception are co-regulated through shared brain regions having bidirectional interplays. Thus, we aimed to investigate whether application of REM sleep deprivation (REM-SD) could affect morphine analgesic tolerance and dependence. To this end, adult male rats underwent sleep deprivation during light and dark phases (LSD and DSD, respectively) using the inverted flower pot method and then tolerance and dependence was induced by repeated injection of morphine for 7 days (10 mg/kg, daily, i.p.). Results indicated that REM-SD delays the development of tolerance to morphine during both phases; however this effect was more potent following LSD. Moreover, LSD decreased the baseline thermal threshold and total withdrawal score. One possible hypothesis for our observations is REM-SD-induced attenuation of orexin system which is still controversial among the researchers. Other stronger possibilities might be down-regulation of opioid receptors in response to sleep loss experience. Finally, it seems that modification of sleep periods may assist to decrease the severity of opioid tolerance and dependence.

Mild regular treadmill exercise ameliorated the detrimental effects of acute sleep deprivation on spatial memory

Vulnerable areas like the hippocampus are sensitive to insults such as sleep deprivation (SD); they are also susceptible to environmental enrichment. Much evidence is accumulating that chronic sleep deprivation causes alterations in the hippocampus that responsible for spatial memory. However, there is conflicting about the differences between acute and chronic SD results. The purpose of this study was to determine the protective effects of mild treadmill exercise on acute SD rats.Four groups were created as control, exercise, sleep deprivation, exercise + sleep deprivation. Multiple platforms method was used to induce REM sleep deprivation (RD) for 48 h. The exercise was applied fivedaysperweekforfour weeks(5 × 4). For the first and second weeks, the length of the exercise was 15 min in two sessions (5 min interval) followed by 15 min in three, 15 min in four sessions. Morris water maze (MWM) was used as a spatial memory test. Gene level was determined by using the qPCR technique. Malondialdehyde (MDA) content in the hippocampus was measured as an extent of peroxidative damage to lipids by using the ELISA method.48 h RD impaired long-term spatial memory significantly. Mild, regular treadmill exercise ameliorated the detrimental effects of acute sleep deprivation on memory. There was no significant difference in MDA between groups. Hippocampal gene expression did not show any changes in all groups.Lack of correlation between memory impairment and levels of genes in the hippocampus is likely to be related to the differences in behavioral and genetic mechanisms.

Flowerpot method for rapid eye movement sleep deprivation does not induce stress as defined by elevated serum corticosterone level in rats

Flowerpot method of rapid eye movement sleep (REMS) deprivation (REMSD) has been most extensively used in experiments to decipher the functions of REMS. The most common but serious criticism of this method has been presumed stress experienced by the experimental animals. The lack of systematic studies with appropriate controls to resolve this issue prompted this study. We have compared serum corticosterone levels as a marker of stress in male rats under REMSD by the flowerpot method and multiple types of control conditions. Additionally, to maintain consistency and uniformity of REMSD among groups, in the same rats, we estimated brain Na-K ATPase activity, which has been consistently reported to increase upon REMSD. The most effective method was one rat in single- or multiple-platforms set-up in a pool because it significantly increased Na-K ATPase activity without elevating serum corticosterone level. More than one rat in multiple platform set-up was ineffective and must be avoided. Also, large platform- and recovery-controls must be carried out simultaneously to rule out non-specific confounding effects.

Impact of REM sleep deprivation and sleep recovery on circulatory neuroinflammatory markers.

ObjectivesSleep loss may contribute to neuroinflammation, which might increase neuroinflammatory markers such as neuron-specific enolase (NSE), creatine kinase-brain fraction (CK-BB), lactate dehydrogenase brain fraction (LDH-BB) in blood. Hence, we evaluated the effect of REM sleep deprivation and recovery on these markers.Material and MethodsTwenty-four adult male Sprague Dawley rats were grouped as control, environmental control, REM sleep deprivation, and 24 hour sleep recovery. The rats were sleep deprived for 72 hours and recovered for 24 hours. NSE, CK-BB, and LDH-BB levels in serum were measured using ELISA.ResultsThe serum NSE, CK-BB, and LDH-BB were significantly higher in 72 hour sleep deprived group compared to control (p<0.01). After 24 hours of sleep recovery, the levels of NSE, CK-BB, and LDH-BB were comparable to control (p>0.05).DiscussionREM sleep deprivation increased serum NSE, CK-BB, and LDH-BB, which might be due to neural damage. However, 24 hours of sleep recovery restored these markers.

A Case Study of Prazosin-Induced Hypothermia

A case report of prazosin-induced hypothermia in a treatment-naive patient with PTSD. A 65-year-old woman with bipolar disorder and nightmares resulting from previous traumas was admitted to an inpatient psychiatry unit for mixed state hypomania and depression with suicidal ideation. Prazosin 1mg was started to help manage nightmares and the patient developed asymptomatic hypothermia with a low of 33.5C after 5 days of therapy. After internal medicine and endocrinology consults and appropriate testing did not result in an explanation, prazosin was stopped and her temperature returned to normal. A rechallenge of prazosin again resulted in a temperature decrease and was then discontinued. Hypothermia is not a reported side effect of prazosin in humans, though one previous case study reports hypothermia with a 20mg total daily dose in the treatment of a patient with hypertension. Animal studies indicate two possible mechanisms of action including 1) increased heat dissipation from skin by inhibition of non-shivering thermogenesis and decreased metabolic rate and 2) temperature increases upon rapid eye movement sleep deprivation (REMSD) in rats by increasing noradrenaline. Prazosin modulates REMSD-induced changes in body temperature in rats by blocking the effects of noradrenaline in postsynaptic receptors. To our knowledge, this is only the second reported case of hypothermia induced by prazosin.

The effect of alpha-2 adrenergic receptors on memory retention deficit induced by rapid eye movement sleep deprivation.

Objective(s): Evidence shows that sleep deprivation (SD) disrupts the formation of hippocampus-related memories. Moreover, α2 adrenergic receptors that are wildly expressed in the CA1 hippocampal region have a significant role in modulating both sleep and memory formation. In the present research, we wanted to investigate the effect of stimulation and blockage of CA1 α2 adrenergic receptors by clonidine (an agonist of α2 adrenergic receptor) and yohimbine (an antagonist of α2 adrenergic receptor), respectively, on memory retention impairment induced by REM SD (RSD) in rats. Materials and Methods:Multiple platform apparatus were used to induce RSD, and the passive avoidance task was used to assess memory consolidation. Clonidine and yohimbine were injected intra-CA1. Results:The results showed that RSD (for 24 and 36, but not 12 hr) decreased memory retention, with no effect on locomotion. Post-training intra-CA1 infusion of a subthreshold dose of yohimbine (0.001 μg/rat) did not alter, while clonidine (0.1 μg/rat) restored memory retention impairment induced by RSD (24 and 36 hr). Also, none of the interventions did not influence locomotor activity. Conclusion:Our data strongly showed that CA1 α2 adrenergic receptors have a critical role in RSD-induced memory retention impairment.

Chronic REM-sleep deprivation induced laryngopharyngeal reflux in rats: A preliminary study

ObjectiveThe aim of this study was to investigate the relationship of chronic REM-sleep deprivation with laryngopharyngeal reflux (LPR) and its mechanism. MethodsForty healthy male SD rats (body weight 250–280 g) were randomly divided into four groups. The first three ones were test group, which underwent REM-sleep deprivation with different duration of time by modified multiplatform water surface method. The last group was the control one having normal sleep. All the animals were performed Dx-pH monitoring when finishing sleep deprivation, and sacrificed to study the gastric residual rate (GRR) and small intestine peristalsis (SPR) rate by charcoal meal method. ResultsAt prone position, the reflux incidence in the test groups fairly increased with the duration of sleep deprivation (p<0.05). The total number of reflux episodes at prone position in the test group rats with 3 months duration of sleep deprivation was significantly increased compared with that in the control ones (p<0.05). GRR in rats experiencing sleep deficiency for different duration all reduced significantly when compared to the control group (p<0.05). GRR and SPR presented continuous decline tendency with the duration of sleep deprivation (p>0.05). ConclusionsIt is suggested that chronic sleep deficiency could cause LPR in rats, which might result from the uncoordinated digestive tract motility caused by dysfunction of central nervous system after chronic REM-sleep deprivation. Our results implied that chronic REM-sleep deprivation might be one of the causes of LPR. Addressing sleep problems might help to decrease the prevalence of LPR and enhance its treatment efficacy.