Effects Of Paradoxical Sleep Deprivation Research Articles

Effects of Paradoxical Sleep Deprivation on MCH and Hypocretin Systems

AbstractMelanin-concentrating hormone (MCH) and hypocretins (Hcrt) 1 and 2 are neuropeptides synthesized in the lateral hypothalamic area by neurons that are critical in the regulation of sleep and wakefulness. Their receptors are located in the same cerebral regions, including the frontal cortex and hippocampus. The present study aimed to assess whether 96 hours of paradoxical sleep deprivation alters the functioning of the MCH and hypocretin systems. To do this, in control rats with normal sleep (CTL) and in rats that were deprived of paradoxical sleep (SD), we quantified the following parameters: 1) levels of MCH and hypocretin-1 in the cerebrospinal fluid (CSF); 2) expression of the prepro-MCH (Pmch) and prepro-hypocretin (Hcrt) genes in the hypothalamus; 3) expression of the Mchr1 and Hcrtr1 genes in the frontal cortex and hippocampus; and 4) expression of the Hcrtr2 gene in the hippocampus. These measures were performed at 6 Zeitgeber time (ZT) points of the day (ZTs: 0, 4, 8, 12, 16, and 20). In the SD group, we found higher levels of MCH in the CSF at the beginning of the dark phase. In the frontal cortex, sleep deprivation decreased the expression of Hcrtr1 at ZT0. Moreover, we identified significant differences between the light and dark phases in the expression of Mchr1 and Hcrtr1, but only in the CTL animals. We conclude that there is a day/night modulation in the expression of components of the MCH and hypocretin systems, and this profile is affected by paradoxical sleep deprivation.

Effects of paradoxical sleep deprivation on oxidative parameters in the serum and brain of mice submitted to the animal model of hyperglycemia

The present study aimed to investigate the effects of paradoxical sleep deprivation (PSD) on behavioral and oxidative stress parameters in the brain and serum of mice submitted to the animal model of hyperglycemia induced by alloxan, mimicking the main symptom of diabetes mellitus (DM). Adults C57BL/6 male and female mice received an injection of alloxan, and ten days later, the animals were submitted to the PSD for 36 h. The animals' behavioral parameters were evaluated in the open-field test. Oxidative stress parameters [Diacetyldichlorofluorescein (DCF), Thiobarbituric acid reactive substances (TBARS), Superoxide dismutase (SOD), and Glutathione] were assessed in the frontal cortex, hippocampus, striatum, and serum. The PSD increased the male and female mice locomotion, but the alloxan's pre-administration prevented the PSD-induced hyperactivity. In addition, the male mice receiving alloxan and submitted to the PSD had elevated latency time in the first quadrant and the number of fecal boli, demonstrating increased anxiety-like behavior. The HPA-axis was hyperactivating in male and female mice pre-administered alloxan and/or PSD-submitted animals. The oxidative stress parameters were also increased in the serum of the animals administered alloxan and/or sleep-deprived mice. Despite alloxan or PSD leading to behavioral or biochemical alterations, the one did not potentiate the other in mice. However, more studies are necessary to identify the link between sleep and hyperglycemia.

Variation in the sexual behavior and blood count parameters induced by sleep deprivation in male rats.

Sleep is a fundamental biological requirement, and lack of sleep has increasingly been recognized to cause metabolic consequences and adversely affect immune function. Recent articles have pointed to how sleep and sexual functions may be interlinked, involving inflammation, vascular alterations, tissue damage, and endothelial dysfunction. We examined the effect of paradoxical sleep deprivation on sexual behavior and hemogram parameters in male rats. In addition, we also explored whether 7 days of recovery sleep is sufficient to offset these detriments. Male rats were given sexual experience through training. At the fifth test, the sexually vigorous males were randomly separated into three experimental groups: paradoxical sleep deprivation (rats submitted to 96h of paradoxical sleep deprivation, n=6), recovery sleep (recovery sleep 7 days after paradoxical sleep deprivation, n=6), and control (n=10). We evaluated the sexual behaviors of three groups. Blood samples were collected to analyze hemogram parameters. In this study, we recognized that repeated copulatory tests can lead to changes in sexual behavior over time. We found that 96h of acute sleep deprivation impaired the sexual behavior of male rats. Our results demonstrated that 96h of paradoxical sleep deprivation also increased levels of white blood cell subpopulations, in particular neutrophils. Recovery sleep after sleep deprivation has a certain reversal effect on white blood cell subgroups and impairment of sexual behavior, with some signs that not all levels were back to baseline even after 7 days of recovery. In general, we found that 96h of paradoxical sleep deprivation impaired the sexual behavior of male rats. Our results demonstrated that paradoxical sleep deprivation can cause systemic inflammation by affecting white blood cell subpopulations, in particular neutrophils. Seven days of recovery sleep after sleep deprivation has a certain reversal effect to these impairments.

Neurochemical effects of sleep deprivation in the hippocampus of the pilocarpine-induced rat model of epilepsy

Objective(s): The present study aims to investigate the pathological mechanisms mediating the effect of paradoxical sleep deprivation (PSD) for 48 hr on the spontaneous recurrent seizures (SRS) stage of the pilocarpine rat model of temporal lobe epilepsy. Materials and Methods: This was carried out through assessment of amino acid neurotransmitter levels, the main oxidative stress parameters, and the levels of tumor necrosis factor-I± (TNF-I±), interleukin-1I² (IL-1I²), and interleukin-6 (IL-6) in the hippocampus. The experimental animals were divided into 4 groups: control, epileptic, PSD, and epileptic㴠 groups.Results: Data indicated that PSD in epileptic rats induced a significant decrease in GSH levels. TNF-I± increased significantly in the PSD group and decreased significantly in both epileptic rats and epileptic rats deprived of paradoxical sleep. PSD induced a significant increase in glutamine, glutamate, and aspartate and a significant decrease in GABA. In epileptic rats and epileptic rats deprived of PS, a significant increase in aspartate and a significant decrease in GABA and taurine were recorded. Â Conclusion: The present data suggest that exposure to PSD for 48 hr did not worsen the alterations produced in the present epileptic model. However, epileptic, PSD, epileptic + PSD groups showed a state of hyperexcitability and oxidative stress. PSD may increase the susceptibility of animals to the development of epilepsy.Â

Neurochemical effects of sleep deprivation in the hippocampus of the pilocarpine-induced rat model of epilepsy

Objective(s):The present study aims to investigate the pathological mechanisms mediating the effect of paradoxical sleep deprivation (PSD) for 48 hr on the spontaneous recurrent seizures (SRS) stage of the pilocarpine rat model of temporal lobe epilepsy. Materials and Methods:This was carried out through assessment of amino acid neurotransmitter levels, the main oxidative stress parameters, and the levels of tumor necrosis factor-α (TNF-α), interleukin-1β (IL-1β), and interleukin-6 (IL-6) in the hippocampus. The experimental animals were divided into 4 groups: control, epileptic, PSD, and epileptic+PSD groups.Results:Data indicated that PSD in epileptic rats induced a significant decrease in GSH levels. TNF-α increased significantly in the PSD group and decreased significantly in both epileptic rats and epileptic rats deprived of paradoxical sleep. PSD induced a significant increase in glutamine, glutamate, and aspartate and a significant decrease in GABA. In epileptic rats and epileptic rats deprived of PS, a significant increase in aspartate and a significant decrease in GABA and taurine were recorded. Conclusion:The present data suggest that exposure to PSD for 48 hr did not worsen the alterations produced in the present epileptic model. However, epileptic, PSD, epileptic + PSD groups showed a state of hyperexcitability and oxidative stress. PSD may increase the susceptibility of animals to the development of epilepsy.

EFFECT OF SLEEP DEPRIVATION ON REMINISCENCE AND APPREHENSION BEHAVIOR IN WISTAR ALBINO RATS

Objective: The aim of the present study is to investigate the effect of paradoxical sleep deprivation (SD) on learning and memory impairment and anxiety-like behavior in female Wistar albino rats.
 Methods: Eight-arm radial maze, open-field test, and light and dark test were used to assess the animals learning and memory and anxiety-like behavior.
 Results: SD associated with weaker learning and memory and increased anxiety- and depressive-like behavior in animals.
 Conclusion: Animals were exposed to SD showed learning and memory impairment and also exhibited increased anxiety- and depressive-like behavior when compared to control animals.

Hippocampal microRNA-191a-5p Regulates BDNF Expression and Shows Correlation with Cognitive Impairment Induced by Paradoxical Sleep Deprivation

The aim of this study was to investigate the effect of paradoxical sleep deprivation (PSD) on the BDNF-related miRNA expression in ovariectomized (OVX) rats. The animals were randomly divided into eight groups (control, PSD, wide platform, sham surgery, anti-miR-191, anti-miR-191/PSD, scrambled and PSD in intact). Bilateral-ovariectomy was performed one month before the experiment in the OVX rats. For the induction of 72 h of PSD, the multiple platform method was applied. The Morris water maze (MWM) test was carried out 30 min after PSD to test spatial learning and memory. Finally, the rats were euthanized 24 h after the last experiment. We quantified miR-10a-5P, miR-10b-5P, miR-125a-3p, miR-155-5p, miR-191a-5p, BDNF and TMOD-2 level using real-time PCR. BNDF protein was also measured by Western blotting. Hippocampal miR-191a and miR-155 were significantly up-regulated (P ˂ .01) and BDNF down-regulated (P ˂ .05) in the PSD group. PSD rats with up-regulated miR-191a swam longer distance and spent more time to find a hidden platform (positive correlation) and showed the lowest percentage of time and distance in the target quadrant (negative correlation). The negative correlation between miR-191a and BDNF levels in the PSD condition provided more evidence for the role of miR-191a in cognitive function. Intracerebroventricular (ICV) injection of anti-miR-191a improved the down-regulation of BDNF and attenuated PSD-induced cognitive impairment. Hippocampal BDNF is probably one of the targets of miR-191a in sleep-deprived OVX rats. Our results suggest that miR-191a may be increased in the sleep-deprived OVX rats to regulate BDNF levels.

Paradoxical Sleep Deprivation Aggravates and Prolongs Incision-Induced Pain Hypersensitivity via BDNF Signaling-Mediated Descending Facilitation in Rats.

The mechanisms underlying the pronociceptive effect of paradoxical sleep deprivation (PSD) are not fully established. The modulation of BDNF signaling-mediated descending facilitation from the rostral ventromedial medulla (RVM) of brain stem has been demonstrated in persistent pain models of inflammatory pain, but not in incisional pain model. Recent study has shown that PSD increases the expression of brain-derived neurotrophic factor (BDNF) in the brainstem structure. Therefore, in the current study, we asked whether the BDNF signaling-mediated descending facilitation was involved in the PSD-induced pronociceptive effect on incisional pain and delay the recovery period of postoperative pain in rats. Our results found that a preoperative 24h PSD significantly aggravated the pain hypersensitivity after incision and prolonged the duration of postoperative pain. The lesions of ipsilateral dorsolateral funiculus partly reversed the PSD-induced pronociceptive effect on incisional pain. Interestingly, the 24h PSD, but not incision significantly enhanced the levels of BDNF protein expression in the RVM areas of rats. Furthermore, at 1day or 4days after incision, intra-RVM microinjection of a BDNF antibody partly reversed the PSD-induced pronociceptive effects in incisional rats, while it did not change the cumulative pain scores and paw withdrawal thresholds in rats receiving only plantar incision. These findings suggest that the preoperative PSD may aggravate and prolong the incision-induced pain hypersensitivity via BDNF signaling-mediated descending facilitation.

Novel environment influences the effect of paradoxical sleep deprivation upon brain and peripheral cytokine gene expression

Sleep loss increases inflammatory mediators in brain and peripheral tissues, but the mechanisms underlying this association are not fully understood. Male C57BL/6j mice were exposed to paradoxical sleep deprivation (PSD) for 24h using the modified multiple platform (MMP) technique (platforms over water) or two different controls: home cage or a dry platform cage, which constituted a novel environment. PSD mice exhibited increased IL-1β and TNF-α pro-inflammatory gene expression in brain (hypothalamus, hippocampus, pre-frontal cortex), as well as in peripheral tissues (liver, spleen), when compared with home-cage controls. In addition, among PSD mice, TGFβ1, an anti-inflammatory cytokine, was increased in pre-frontal cortex, liver, and spleen in conjunction with elevated serum corticosterone concentration relative to home-cage controls. However, these differences were nearly abolished when PSD mice were compared with control mice subjected to a dry MMP cage, suggesting that simply exposing mice to a novel environment can induce an acute inflammatory response.

The dual effect of paradoxical sleep deprivation on murine immune functions

We aimed to evaluate the effect of paradoxical sleep deprivation on the cellular migration during inflammation, the peritoneal macrophage phenotype and the infectious stimulus outcomes. A/J mice were inoculated with thioglycollate and exposed to paradoxical sleep deprivation. Sleep-deprived animals presented decreased cell migration compared to controls. Nitric oxide production was reduced in macrophages from sleep-deprived mice compared to controls. Cell surface analysis showed that sleep deprivation reduced F4/80+/CD80low peritoneal cell population induced by thioglycollate injection. Sleep-deprived mice were not more susceptible to infection than control mice. Our findings challenge the general perception that sleep loss always increases infection susceptibility.

Paradoxical sleep deprivation impairs mouse survival after infection with malaria parasites.

BackgroundParasitic diseases like malaria are a major public health problem in many countries and disrupted sleep patterns are an increasingly common part of modern life. The aim of this study was to assess the effects of paradoxical sleep deprivation (PSD) and sleep rebound (RB) on malarial parasite infection in mice.MethodsAfter PSD, one group was immediately infected with parasites (PSD). The two other PSD rebound groups were allowed to sleep normally for either 24 h (24 h RB) or 48 h (48 h RB). After the recovery periods, mice were inoculated with parasites.ResultsThe PSD group was the most affected by parasites presenting the higher death rate (0.02), higher number of infected cells (p < 0.01), and decrease in body weight (p < 0.04) compared to control and 48 h RB groups. The 24 h RB group was also different from control group in survival (p < 0.03), number of infected cells (p < 0.05) and body weight (p < 0.04). After 48 hours of sleep rebound animals were allowed to restore their response to parasitic infection similar to normal sleep animals.ConclusionsThese results suggest that PSD is damaging to the immune system and leads to an increased infection severity of malaria parasites; only 48 hours of recovery sleep was sufficient to return the mice infection response to baseline values.Electronic supplementary materialThe online version of this article (doi:10.1186/s12936-015-0690-7) contains supplementary material, which is available to authorized users.

The Pronociceptive Effect of Paradoxical Sleep Deprivation in Rats: Evidence for a Role of Descending Pain Modulation Mechanisms.

The mechanisms underlying the pronociceptive effect of paradoxical sleep deprivation (PSD) are not known. In this study, we asked whether PSD increases tonic nociception in the formalin test, decreases the antinociceptive effect of morphine administered into the periaqueductal gray matter (PAG), and disrupts endogenous descending pain modulation. PSD for either 24 or 48 h significantly increased formalin-induced nociception and decreased mechanical nociceptive paw withdrawal threshold. The maximal antinociceptive effect induced by morphine (0.9-9 nmol, intra-PAG) was significantly decreased by PSD. The administration of a low dose of the GABAA receptor antagonist, bicuculline (30-300 pmol, intra-PAG), decreased nociception in control rats, but not in paradoxical-sleep-deprived ones. Furthermore, the administration of the cholecystokinin (CCK) 2 receptor antagonist, YM022 (0.5-2 pmol) in the rostral ventral medulla (RVM), decreased nociception in paradoxical-sleep-deprived rats but not in control ones. While a dose of the CCK 2 receptor agonist, CCK-8 (8-24 pmol intra-RVM), increased nociception in control rats, but not in paradoxical-sleep-deprived ones. In addition, the injection of lidocaine (QX-314, 2%, intra-RVM) decreased nociception in sleep-deprived rats, but not in control rats, while the lesion of the dorsolateral funiculus prevented the pronociceptive effect of PSD. Finally, PSD significantly increased c-Fos expression in the RVM. Therefore, PSD increases pain independently of its duration or of the characteristic of the nociceptive stimulus and decreases morphine analgesia at the PAG. PSD appears to increase pain by decreasing descending pain inhibitory activity and by increasing descending pain facilitatory activity.

The effects of paradoxical sleep deprivation on amphetamine-induced behavioral sensitization in adult and adolescent mice

Drug-induced behavioral sensitization (BS), paradoxical sleep deprivation (PSD) and adolescence in rodents are associated with changes in the mesolimbic dopaminergic system. We compared the effects of PSD on amphetamine-induced BS in adult and adolescent mice. Adult (90 days old) and adolescent (45 days old) Swiss mice were subjected to PSD for 48h. Immediately after PSD, mice received saline or 2.0mg/kg amphetamine intraperitoneally (i.p.), and their locomotion was quantified in activity chambers. Seven days later, all the animals were challenged with 2.0mg/kg amphetamine i.p., and their locomotion was quantified again. Acute amphetamine enhanced locomotion in both adult and adolescent mice, but BS was observed only in adolescent mice. Immediately after its termination, PSD decreased locomotion of both saline- and amphetamine-treated adolescent mice. Seven days later, previous PSD potentiated both the acute stimulatory effect of amphetamine and its sensitization in adolescent mice. In adult animals, previous PSD revealed BS. Our data suggest that adolescent mice are more vulnerable to both the immediate and long-term effects of PSD on amphetamine-induced locomotion. Because drug-induced BS in rodents shares neuroplastic changes with drug craving in humans, our findings also suggest that both adolescence and PSD could facilitate craving-related mechanisms in amphetamine abuse.

Differential effects of paradoxical sleep deprivation on memory and oxidative stress

Sleep has important functions for every organ in the body and sleep deprivation (SD) leads to disorders that cause irreparable damage. The aim of this study was to investigate behavioral and brain structural alterations in mice deprived of paradoxical sleep for 48 and 72 h. Working memory, aversive memory as well as levels of nitric oxide (NO) and thiobarbituric acid reactive substances (TBARS) in the hippocampus, body striatum, and prefrontal cortex were evaluated. Working memory was affected in the 48- and 72-h SD groups while aversive memory was altered only in the 48-h SD group (p ≤ 0.05). Our findings showed that SD reduces NO levels in most brain areas (p < 0.05): NO levels were unaltered in the striatum of animals sleep-deprived for 48 h. Higher levels of TBARS were observed in all areas of the SD groups (p ≤ 0.05). Thus, we confirmed that SD has duration-dependent effects on behavior as well as on NO and TBARS levels in the brain. Preserved striatum NO levels suggest that this structure is less vulnerable to oxidative stress and is only affected by SD of longer duration. Increased TBARS and reduced NO levels in the hippocampus and prefrontal cortex confirm a central role for both these structures in working memory and aversive memory. Contextual fear conditioning was not affected by longer periods of SD. Thus, our findings suggest that shorter SD time may be more beneficial to avoid aversive memory where this may have implications for the management of posttraumatic stress.

Aerobic exercise attenuates inhibitory avoidance memory deficit induced by paradoxical sleep deprivation in rats

The deleterious effects of paradoxical sleep deprivation (SD) on memory processes are well documented. Physical exercise improves many aspects of brain functions and induces neuroprotection. In the present study, we investigated the influence of 4 weeks of treadmill aerobic exercise on both long-term memory and the expression of synaptic proteins (GAP-43, synapsin I, synaptophysin, and PSD-95) in normal and sleep-deprived rats. Adult Wistar rats were subjected to 4 weeks of treadmill exercise training for 35min, five times per week. Twenty-four hours after the last exercise session, the rats were sleep-deprived for 96h using the modified multiple platform method. To assess memory after SD, all animals underwent training for the inhibitory avoidance task and were tested 24h later. The aerobic exercise attenuated the long-term memory deficit induced by 96h of paradoxical SD. Western blot analysis of the hippocampus revealed increased levels of GAP-43 in exercised rats. However, the expression of synapsin I, synaptophysin, and PSD-95 was not modified by either exercise or SD. Our results suggest that an aerobic exercise program can attenuate the deleterious effects of SD on long-term memory and that this effect is not directly related to changes in the expression of the pre- and post-synaptic proteins analyzed in the study.

Changes in gene expression in the frontal cortex of rats with pilocarpine-induced status epilepticus after sleep deprivation

Sleep and epilepsy present a bidirectional interaction. Sleep complaints are common in epilepsy, and sleep deprivation may provoke seizures. However, the mechanisms underlying this relationship are unknown. Thus, this study investigated the effects of paradoxical sleep deprivation (PSD24h) and total sleep deprivation (TSD6h) in the expression of genes related to reactive oxygen species and nitric oxide production in the frontal cortex of a rodent model of temporal lobe epilepsy (PILO). The data show that PILO rats had increased NOX-2 expression and decreased SOD expression, independent of sleep. Higher NOX-2 expression was observed only in PILO rats subjected to the control condition and TSD6h. Also, eNOS and DDAH1 were increased in the PILO group submitted to TSD6h. Moreover, CAT expression in the frontal cortex of PILO rats submitted to PSD24h was reduced compared to that of PILO rats that were not sleep-deprived. The molecular changes found in the frontal cortex of PILO rats following sleep deprivation suggest a mechanism via oxidative stress.

More than hormones: Sex differences in cardiovascular parameters after sleep loss in rats

Although the influence of sex on sleep pattern and cardiovascular parameters is well known, knowledge regarding the effects of sleep loss on heart responses in both sexes is scarce. The present study investigated the effects of paradoxical sleep deprivation (PSD) and chronic sleep restriction (SR) on cardiovascular parameters and adrenocorticotropic hormone (ACTH) levels in male and female rats. Both groups were randomly assigned to PSD for 96 h, SR for 21 days or home-cage control. Mean arterial pressure (MAP), heart rate (HR), baroreflex sensitivity (bradycardia and tachycardia responses) and ACTH levels were evaluated. The results showed that PSD induced a significant increase in HR and ACTH levels in both sexes, although male rats presented higher levels of ACTH hormone compared to females. In addition to sex-specific responses, PSD decreased the tachycardia only in male rats. SR, induced a significant increase in MAP and decrease in bradycardia in both sexes. Male rats were more affected by sleep deprivation protocols than females for MAP, bradycardia response, and ACTH levels. The results showed that the effects of sleep loss on cardiovascular parameters are associated with the protocol of sleep deprivation and that sex can modulate these effects. We suggested this experimental model as a suitable tool for further investigations of the relationship between cardiovascular parameters and sleep.

Paradoxical sleep deprivation potentiates epilepsy induced by homocysteine thiolactone in adult rats

There is an intriguing and still poorly understood relationship between sleep deprivation and epilepsy. It has recently been shown that paradoxical sleep deprivation decreases levels of homocysteine, an amino acid involved together with its thiolactone metabolite in epileptogenesis. The aim of the present study was to investigate the effects of paradoxical sleep deprivation on homocysteine thiolactone (H)-induced seizures in rats, a model of generalized seizures. Selective deprivation of paradoxical sleep in adult male Wistar rats was achieved by the platform method. Animals with implanted electrodes for electroencephalogram (EEG) registration were assigned to appropriate experimental conditions (dry cage for control, large platform for stress control and small platform for paradoxical sleep deprivation) and 72 h later were intraperitoneally treated with either H (5.5 mmol/kg) or saline (0.9% NaCl). This study showed that paradoxical sleep deprivation increased the incidence and number of H-induced seizure episodes, shortened latency time to seizures and led to significant rates of lethality after H administration, but without effect on the seizure severity. Paradoxical sleep deprivation increased the number and duration of spikes-and-wave discharges, while decreased latency to its appearance in EEG. Judging by the behavioral and EEG findings, it could be concluded that paradoxical sleep deprivation can provoke the expression of factors that can potentiate H-induced seizures in adult rats.

Sleep deprivation impairs emotional memory retrieval in mice: Influence of sex

The deleterious effects of paradoxical sleep deprivation on memory processes are well documented. However, non-selective sleep deprivation occurs more commonly in modern society and thus represents a better translational model. We have recently reported that acute total sleep deprivation (TSD) for 6 h immediately before testing impaired performance of male mice in the plus-maze discriminative avoidance task (PM-DAT) and in the passive avoidance task (PAT). In order to extend these findings to females, we examined the effect of (pre-test) TSD on the retrieval of different memory tasks in both male and female mice. Animals were tested using 3 distinct memory models: 1) conditioning fear context (CFC), 2) PAT and 3) PM-DAT. In all experiments, animals were totally sleep-deprived by the gentle interference method for 6h immediately before being tested. In the CFC task and the PAT, TSD induced memory impairment regardless of sex. In PM-DAT, the memory impairing effects of TSD were greater in females. Collectively, our results confirm the impairing effect of TSD on emotional memory retrieval and demonstrate that it can be higher in female mice depending on the memory task evaluated.

Female rats are more susceptible to the deleterious effects of paradoxical sleep deprivation on cognitive performance

Paradoxical sleep deprivation (PSD) may alter subsequent learning and memory capacity. There are differences in both the intensity and direction of responses of the male and female species to the same environmental stimuli and experimental conditions. In the present study, we examined the extent of the effects of PSD for 72h on spatial learning and memory, anxiety-like behavior, corticosterone levels, and the body weight in male as well as in intact and ovariectomized (OVX) female Wistar rats. Multiple platform method was used for PSD induction. Spatial learning and memory and anxiety-like behavior were determined using Morris water maze (MWM) task and open field test, respectively. The data showed that PSD could not significantly affect subsequent spatial learning and short-term memory in male rats, while it significantly impaired the performance of the intact and OVX female rats. The PSD-intact and -OVX female rats showed more memory impairment than the PSD-male animals. Those impairments do not appear to be due to elevated stress level, since the plasma corticosterone did not significantly change following PSD induction. The open field data showed that PSD significantly reduced anxiety-like behavior in all experimental groups. In addition, PSD had a reducing effect on the mean body weight of female groups. Such results suggest that the female rats are more vulnerable to the deleterious effects of sleep loss on cognitive performance.