Effects of fornix lesions on waking and sleep patterns in white rats.

Polygraphic 12-hr daytime observation of male albino rats revealed increased spontaneous motor activity by a coronal fornical transection but not by a frontal cortical lesion. Fornicotomy alone affected sleep patterns by reducing the total time spent in slow wave sleep (SWS) and paradoxical sleep (PS) and in frequency of occurrence of SWS and PS and by increasing mean duration in the PS phase and the inter PS-interval. However, fornicotomy failed to affect the ratio of the two sleep phases (PS/SWS) either in total time, frequency of occurrence or duration and it did not alter the rate of tiny muscle twitching in PS. Since hippocampal theta activity was completely eliminated by the fornix lesions, the previously hypothesized relationship between theta activity and behaviors such as voluntary movement and PS is in need of revision.     

Effects of Sleep Deprivation on Memory and Sleep Latencies in Connection with Repeated Awakenings From Sleep

Twelve subjects were kept awake 64 hrs. During baseline and recovery sleep, subjects were given a simple memory task. The subjects were awakened 3 times each night during slow-wave sleep and shown 4 playing cards. Approximately 90 min later the subjects were again awakened and tested for retention of the previous cards and given 4 new cards to learn. This procedure was repeated 3 times each night and upon awakening the following morning. On the recovery night recall was reduced, slow-wave sleep was lengthened, sleep latency was shortened, and body motility was reduced. It was suggested that the reason for the poorer recall was deeper sleep induced by the sleep deprivation.     

Brain temperature variations during natural sleep and arousal in white rats

In 15 free moving white rats brain temperature (in sensorimotor cortical area), dorsal hippocampal and neocortical EEG and EMG of the neck muscles were recorded. It was found that total (neocortical and hippocampal) EEG desynchronization per se (during slow wave sleep, in EEG arousal without behavioral activiation, in passive avoidance responses) was not capable of eliciting a brain temperature rise and frequently (especially during slow wave sleep) led to its decrease. Brain temperature was found to increase upon the appearance of distinct synchronization of the regular hippocampal rhythm (during fast sleep phase, in behavioral arousal with orienting and exploratory responses). Cyclic increases in synchronization of slow waves and spindles divided by short-term desynchronization periods (slow sleep microcycles) were accompanied by small but distinct temperature elevations on the background of slow temperature fall or plateau.     

Sleep deprivation lowers reactive aggression and testosterone in men

The role of sleep deprivation in aggressive behavior has not been systematically investigated, despite a great deal of evidence to suggest a relationship. We investigated the impact of 33 h of sleep loss on endocrine function and reactive aggression using the Point Subtraction Aggression Paradigm (PSAP) task. PSAP performance was assessed in 24 young men and 25 women who were randomly assigned to a sleep deprivation or control condition. Sleep deprivation lowered reactive aggression and testosterone (but not cortisol) in men, and disrupted the positive relationship between a pre-post PSAP increase in testosterone and aggression that was evident in rested control men. While women increased aggression following provocation as expected, no influence of sleep deprivation was found. This is the first experimental study to demonstrate that sleep deprivation lowers reactive aggression in men. Testosterone, but not cortisol, played a role in the relationship between sleep and reactive aggression in men.     

Sleep deprivation alters pupillary reactivity to emotional stimuli in healthy young adults

The aim of this pilot study was to quantify the impact of sleep deprivation on psychophysiological reactivity to emotional stimuli. Following an adaptation night of sleep in the lab, healthy young adults were randomly assigned to either one night of total sleep deprivation or to a normal sleep control condition. The next afternoon, responses to positive, negative, and neutral picture stimuli were examined with pupillography, an indicator of cognitive and affective information processing. Only the sleep-deprived group displayed significantly larger pupil diameter while viewing negative pictures compared to positive or neutral pictures. The sleep-deprived group also showed anticipatory pupillary reactivity during blocks of negative pictures. These data suggest that sleep deprivation is associated with increased reactions to negative emotional information. Such responses may have important implications for psychiatric disorders, which may be triggered or characterized by sleep disturbances.     

Sleep deprivation and neurobehavioral functioning in children

Sleep deprivation can result in significant impairments in daytime neurobehavioral functioning in children. Neural substrates impacted by sleep deprivation include the prefrontal cortex, basal ganglia and amygdala and result in difficulties with executive functioning, reward anticipation and emotional reactivity respectively. In everyday life, such difficulties contribute to academic struggles, challenging behaviors and public health concerns of substance abuse and suicidality. In this article, we aim to review 1) core neural structures impacted by sleep deprivation; 2) neurobehavioral problems associated with sleep deprivation; 3) specific mechanisms that may explain the relationship between sleep disturbances and neurobehavioral dysfunction; and 4) sleep problems reported in common neurodevelopmental disorders including attention deficit hyperactivity disorder (ADHD) and autistic spectrum disorders (ASDs).     

Sleep deprivation of rats: the hyperphagic response is real

STUDY OBJECTIVES: Chronic sleep deprivation of rats causes hyperphagia without body weight gain. Sleep deprivation hyperphagia is prompted by changes in pathways governing food intake; hyperphagia may be adaptive to sleep deprivation hypermetabolism. A recent paper suggested that sleep deprivation might inhibit ability of rats to increase food intake and that hyperphagia may be an artifact of uncorrected chow spillage. To resolve this, a palatable liquid diet (Ensure) was used where spillage is insignificant. DESIGN: Sleep deprivation of male Sprague Dawley rats was enforced for 10 days by the flowerpot/platform paradigm. Daily food intake and body weight were measured. On day 10, rats were transcardially perfused for analysis of hypothalamic mRNA expression of the orexigen, neuropeptide Y (NPY). SETTING: Morgan State University, sleep deprivation and transcardial perfusion; University of Maryland, NPY in situ hybridization and analysis. MEASUREMENTS AND RESULTS: Using a liquid diet for accurate daily measurements, there was no change in food intake in the first 5 days of sleep deprivation. Importantly, from days 6-10 it increased significantly, peaking at 29% above baseline. Control rats steadily gained weight but sleep-deprived rats did not. Hypothalamic NPY mRNA levels were positively correlated to stimulation of food intake and negatively correlated with changes in body weight. CONCLUSION: Sleep deprivation hyperphagia may not be apparent over the short term (i.e., < or = 5 days), but when extended beyond 6 days, it is readily observed. The timing of changes in body weight and food intake suggests that the negative energy balance induced by sleep deprivation prompts the neural changes that evoke hyperphagia.     

Septal driving of hippocampal theta rhythm as a function of frequency in the infant male rat

Summary The threshold current of septal stimulation required to drive the hippocampal theta rhythm was investigated as a function of stimulation frequency in male rats aged 12–19 days. The minimum in the threshold-frequency function at 7.7 Hz, characteristic of adult male rats, appeared at 15–16 days. Before that age the relation between frequency and threshold was monotonic, as in adult female rats.     

海马区神经电信号相位同步化的初步研究

大脑各个区域的神经电活动存在各种不同频率的振荡,而theta节律振荡(5～10 Hz)是海马区神经活动具有代表性的特征.本文用海马区theta节律显著性检测和theta节律相位同步化的方法来分析多电极记录的神经元放电及其局部场电位信号,验证了theta节律成分的显著性和动物行为之间的关系,并首次研究了小鼠在不同行为状态下左右海马神经电活动之间的相位同步化的差异.     

Effects of sustained manual work and partial sleep deprivation on muscular strength and endurance

Summary In a military field artillery trial, the effects of 8 days of sustained manual work and partial sleep loss on isometric right hand grip strength and upper and lower body anaerobic power (using the Wingate test) was investigated in 25 healthy young male soldiers. During the trial, the physical activity of each subject was essentially identical except that an experimental group (n=18) manually handled a large quantity of artillery shells (weighing 45 kg) and charges (13 kg), whilst a control group (n=7) merely simulated manual handling activities and did no lifting or loading of shells. The daily amount of sleep obtained by each group was similar (3 to 4 hours), as were their activity patterns and food and fluid intake. Isometric right hand grip strength for both groups fell progressively during the trial and did not return to pre-trial levels during 3 days of recovery. At the end of the 8 day trial, there were statistically significant reductions in the body weight (1.9%,p< 0.001), % body fat (7.1%,p< 0.001) and upper body mean power (7.3%,p<0.01) of the experimental group but not in the controls. Lower body peak and mean power were significantly increased at the end of the trial in both the experimental (14.7%,p<0.001 and 17.0%,p<0.001 respectively) and control (14.3%,p<0.01 and 15.0%,p<0.05 respectively) groups. Lower body power decrease was significantly increased (18.1%,p<0.05) in the experimental group but not in the controls. It is suggested that the increase in lower body anaerobic power may be associated with the increased level of physical activity during the trial ie a training effect, and that the decrease in upper body anaerobic power may be associated with the combination of unaccostomed arduous manual handling of heavy loads and partial sleep loss since it was only observed in the experimental group.     

EEG spectral power and cognitive performance during sleep inertia: the effect of normal sleep duration and partial sleep deprivation

Sleep inertia (SI) is a transient period occurring immediately after awakening, usually characterized by performance decrement. When sleep is sufficient, SI is moderate, and produces few or no deficit. When it is associated with prior sleep deprivation, SI shows dose-dependent negative effects on cognitive performance, especially when subjects have been awaken in slow wave sleep (SWS). In the present study, spectral analysis was applied during the last 10 min before and the first 10 min after awakening, and during 1 h after awakening while subjects performed the Stroop test. Seventeen subjects were divided into a Control group who slept 8 h, and a Sleep Deprived group who slept only 2 h. The results show that performance was normal in the Control group, whereas reaction time was increased during the first half hour and error level during the second half hour in the Sleep Deprived group. Spectral analysis applied on the waking EEG during the whole test session showed that alpha activity was increased in both groups, but theta power only in the Sleep Deprived group. There was a high positive correlation in sleep deprived subjects between delta power during the last 10 min of sleep and subsequent performance decrement in speed and accuracy. Comparison of individual records showed a high positive correlation between spectral power before and after awakening in the Control group (generally in the sense of an increased frequency band), but no correlation was found in the Sleep Deprived group who exhibited a rather disorganized pattern. We discuss these results in terms of incoherence in the EEG continuity during sleep offset after prior sleep loss, which could partly account for the performance decrement observed during SI in sleep deprived subjects.     

Sleep deprivation affects the sensitivity of proactive and reactive action monitoring: A behavioural and ERP analysis

We studied the impact of sleep deprivation on action monitoring. Each participant performed a Simon task after a normal night of sleep and after 26 h of awakening. Reaction time (RT) distributions were analyzed and the sensitivity of the error negativity (Ne/Ne like) to response correctness was examined.     

Sleep patterns in the owl Strix aluco

In two owls the occurrence of paradoxical sleep was tested both behaviorally and electrographically. The waking and sleeping states of the owl can be clearly distinguished. Sleep consisted of two phases: a phase covering most of the sleep which is characterized by motionless posture, slow high-voltage EEG waves, reduced EMG activity of the neck muscles compared with the waking EMG, tonic bradycardia, reduced respiration rate and absence of eye movements; a phase occurring periodically, which is characterized by motionless posture, complete eyelid closure, absence of eye movements, presence of tonic EMG activity and by low voltage fast EEG pattern. Occasionally, this phase of sleep was associated with cardiac irregularities, respiratory apnea and gross body twitches. Thus this phase of sleep was considered to be analogous to the paradoxical sleep of mammals.     

Sleep deprivation and daily torpor impair object recognition in Djungarian hamsters

Sleep has been shown to play a facilitating role in memory consolidation, whereas sleep deprivation leads to performance impairment both in humans and rodents. The effects of 4-h sleep deprivation on recognition memory were investigated in the Djungarian hamster (Phodopus sungorus). Because sleep during the first hours after daily torpor has many similarities to recovery from sleep deprivation, the effects of spontaneous torpor on object recognition were also assessed. A 4-h sleep deprivation, starting immediately after an object learning task, diminished the ability of the hamsters to: (1) discriminate between an already encountered object (target) and a novel object presented in a novel context, (2) retrieve a target within a complex spatial scene, and (3) detect a spatial rearrangement of familiar objects in a familiar context. Plasma stress hormone levels were similar in sleep-deprived and control hamsters. The occurrence of a daily torpor episode during retention was associated with impaired old-new object discrimination performance in the more effortful complex spatial scene task only, and in a two-object choice situation in a novel context no torpor-induced deficit was found. Our results show that post learning sleep deprivation and daily torpor induce a deficit in familiar object retrieval performance in a complex spatial scene, while sparing familiarity-based recognition and novelty processing. Sleep deprivation during the first 4 h of memory consolidation hampered also recency memory for discrete objects. Stress was not a factor contributing to the sleep deprivation-induced impairment.     

Intraseptal infusion of selective and competitive glutamate receptor agonist NMDA and antagonist d-2-amino-5-phosphonopentanoic acid spectral implications for the physostigmine-induced hippocampal theta rhythm in urethane-anesthetized rats

Theta () rhythm may be mediated, at least in part, by a glutamate neurotransmitter. Thus, in the present study, it was hypothesized that the septum glutamatergic NMDA receptor subtype may be involved in the modulation of physostigmine-induced rhythm. To test this hypothesis, we analyzed, in the urethane-anesthetized rat, the effects of septum application of NMDA and d-2-amino-5-phosphonopentanoic acid (AP5), selective and competitive NMDA agonist and antagonist, respectively, on the spectral characteristics of hippocampal rhythm elicited by intravenous injection of a anticholinesterase agent, physostigmine. A low dose (16 nmol) of AP5 did not significantly affect EEG recordings, whereas a high dose (50.75 nmol) resulted in significant decreases in phase (-61.8%) at frequency, peak power (-64.2%), and absolute power of the low-frequency band (-67%). These electroencephalographic alterations, which appeared at 50.75 nmol AP5, were amplified following application of massive doses of the drug (121.8 nmol, n=1, and 162 nmol, n=1). Amplification, however, was slight and the waves remained clearly detectable. On the other hand, the infusion of NMDA resulted in a significant increase in frequency (+25%) of this rhythm, but this effect was completely antagonized by prior local administration of 16 nmol AP5. Our data suggest that the septal NMDA receptors exert subtle modulatory influences on the septohippocampal cells involved in physostigmine-induced wave production, which has not been reported elsewhere: tonic with respect to both low-frequency band power and phase, and phasic with respect to frequency. Our data also indicate that the septum may be a sensitive action site for exogenously administered glutamatergic drugs.     

The effect of a REM sleep deprivation procedure on different aspects of memory function in humans

Previous studies have suggested that memory is dependent on the occurrence of REM sleep. Research has mainly focused on two distinct types of memory function, declarative and procedural, and it seems that the latter may more directly depend on REM sleep. Memory consolidation has been more investigated than acquisition, maintenance, and recall, despite the fact that sleep may affect flow of information into/from storage. Moreover, tests have often been limited to stimuli within only one modality (usually visual or verbal). This study aimed to clarify the role of REM sleep in memory by investigating aspects of memory function, processing, and modality in the same experimental setting. Tests of acquisition and consolidation of multiple aspects of memory function within the visual and verbal modalities were administrated to subjects before and after REM sleep deprivation. Results show that test performance was not affected by REM sleep deprivation.     

Sleep deprivation blunts the night time increase in aldosterone release in humans

The aim of this study was to determine the effect of sleep deprivation on the 24-h profile of aldosterone and its consequences on renal function. Aldosterone and its main hormonal regulatory factors, ACTH (evaluated by cortisol measurement) and the renin-angiotensin system [RAS, evaluated by plasma renin activity (PRA) measurement] were determined every 10 min for 24 h in eight healthy subjects in the supine position, once with nocturnal sleep and once during total 24-h sleep deprivation. Plasma Na(+) and K(+) were measured every 10 min in four of these subjects. In an additional group of 13 subjects under enteral nutrition, diuresis, natriuresis and kaliuresis were measured once during the sleep period (23.00--07.00 h) and once during a 23.00--07.00 hours sleep deprivation period. During sleep deprivation, aldosterone displayed lower plasma levels and pulse amplitude in the 23.00--07.00-hour period than during sleep. Similarly, PRA showed reduced levels and lower pulse frequency and amplitude. Plasma cortisol levels were slightly enhanced during sleep deprivation. Overnight profiles of plasma K(+) and Na(+) were not affected. Diuresis and kaliuresis were not influenced by sleep deprivation. In contrast, natriuresis significantly increased during sleep deprivation. This study demonstrates that sleep deprivation modifies the 24-h aldosterone profile by preventing the nocturnal increase in aldosterone release and leads to altered overnight hydromineral balance.     

Effects of sleep deprivation on behaviors and abnormal hippocampal BDNF/miR-10B expression in rats with chronic stress depression

Being sleep-deprived can relieve the depressed emotions in rats, but the underlying mechanisms remain unknown. In this study, male rats were divided into 3 groups: normal control (NC), chronicunpredictable stress (CUPS) and sleep-deprived (SD). All of the groups were examined using the sucrose consumption test and the open field test. The sucrose consumption test and the open field test were performed for all three groups. The BDNF and miR-10B expressions were examined using real-time PCR and the level of BNDF was discovered by western blotting. In the sucrose consumption test and the open field test, the CUPS rats consumed less sucrose and got fewer score than the NC rats, however the SD rats consumed significantly more sucrose and received higher scores than the CUPS rats. Both the expression of BNDF and the protein levels in the CUPS group was significantly lower than in the NC group. Also, the CUPS group also showed a higher miR-10B expression than the NC group. However, the SD group demonstrated higher BDNF expression and lower miR-10B expression when compared with the CUPS group. Further investigation demonstrated that the BDNF is the direct target gene of miR-10B and BDNF expression, which is negatively correlated with the expression of miR-10B. In the sucrose consumption test, BNDF expression is positively correlated with the sucrose preference rate whereas miR-10B has an opposing correlation. Moreover, the open field test demonstrated that BNDF expression is positively correlated with the scores and the miR-10B expression is negatively correlated. These results indicate that sleep deprivation is closely linked with the downregulation of miR-10B and possibly the upregulation of BDNF in the hippocampus in the CUPS rats.     

Sleep Disruption Aggravates Focal Cerebral Ischemia in the Rat

Study Objectives:

Sleep changes are frequent in stroke patients and predict a poor outcome. It remains unclear how sleep influences stroke evolution and recovery. We assessed effects of sleep disruption on brain damage and on the expression of axon sprouting genes after focal cerebral ischemia in rats.

Design:

12 h after ischemia induced by occlusion of the middle cerebral artery, rats were subjected to sleep disruption including sleep deprivation for 12h (SDpv12h) and sleep disturbances (SDis) by SDpv12h for consecutive 3 days. Control groups included ischemia without SDpv12h or SDis, sham surgery plus SDis and sham surgery without SDis. Sleep changes were evaluated based on EEG and EMG recordings.

Measurements and Results:

SDpv12h increased the infarct volume by 40% (SDpv12h 82.8 ± 10.9 vs. control 59.2 ± 13.9 mm³, P = 0.008) and SDis by 76% (SDis 58.8 ± 20.4 vs. control 33.8 ± 6.3 mm³, P = 0.017). SDpv12h also increased the number of damaged cells, visualized by TUNEL staining, by 137% (SDpv12h 46.8 ± 15 vs. control 19.7 ± 7.7/mm², P < 0.001) and SDis by 219% (SDis 32.9 ± 13.2 vs. control 10.3 ± 2.5/mm², P = 0.002). In addition, SDis significantly elevated the expression of the axonal extension inhibitory molecule neurocan (SDis 14.3 ± 0.4 vs. control 6.2 ± 0.1-fold of change, P < 0.001) in the injured hemisphere.

Conclusions:

These results provide the first direct evidence for a detrimental impact of sleep disruption on stroke evolution and suggest a potential role of sleep modulating treatments on stroke outcomes.

Citation:

Gao B; Cam E; Jaeger H; Zunzunegui C; Sarnthein J; Bassetti CL. Sleep disruption aggravates focal cerebral ischemia in the rat. SLEEP 2010;33(7):879-887.     

Sleep homeostasis in the rat: Simulation of the time course of EEG slow-wave activity

According to the two-process model of sleep regulation, a homeostatic Process S increases during waking and declines during sleep. For humans, the time course of S has been derived from the changes in EEG slow-wave activity (SWA; spectral power density in the 0.75–4.0 Hz range) during sleep. We tested the applicability of the model to sleep in the rat. The simulation was based on the vigilance states for consecutive 8-s epochs of a 96-h experiment in 9 animals. The level of S was made to decrease in epochs of non-REM sleep (NREMS), and to increase in epochs of waking or REM sleep according to exponential functions. By optimizing the initial value and the time constants of S, a close fit between the hourly values of SWA in NREMS and of S was obtained. The biphasic time course of SWA during baseline, its enhancement in the initial recovery period after 24-h sleep deprivation, and its subsequent prolonged undershoot were present in the simulation. We conclude that sleep homeostasis as conceptualized in the two-process model may be a general property of mammalian sleep.