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PubMed1996

Are physiological effects of sleep deprivation in the rat mediated by bacterial invasion?

Recent reports have indicated that rats subjected to total sleep deprivation (TSD) by the disk-over-water method and sacrificed when death appeared imminent showed aerobic bacteria in their blood. Yoked control rats did not. Extrapolating from these results, it has been suggested that the late body temperature declines and eventual deaths of TSD rats are caused by septicemia, and that other, earlier-appearing effects of TSD-including weight loss, increased energy expenditure, and regulation of temperature at a higher level-might be mediated by impaired host defenses against bacterial invasion. Three measures of aerobic bacterial invasion were used to evaluate these hypotheses: bacteremia, bacterial colonization in major organs of filtration (liver, kidney, and mesenteric lymph nodes), and adherence of bacteria to the cecal wall. Experiment 1 showed nonsignificant trends toward more bacterial invasion in 4-day TSD rats compared to yoked control rats and no relationship between the bacterial indicators and the early TSD effects. Experiment 2 showed that the elimination of aerobic bacterial infection by antibiotic treatment did not prevent the early TSD effects in 4-day TSD rats. Experiment 3 showed that the elimination of aerobic bacterial invasion in TSD rats did not eliminate the late temperature decline or the progression towards death. The results showed no significant evidence of aerobic bacterial invasion early in TSD and no indication that the major effects of TSD were dependent upon aerobic bacterial invasion.

Animals↗
PubMed2005

The diurnal rhythm of the cytoprotective human trefoil protein TFF2 is reduced by factors associated with gastric mucosal damage: ageing, Helicobacter pylori infection, and sleep deprivation.

OBJECTIVES: To determine if the normal TFF2 diurnal rhythm is disrupted in those with increased risk of gastric morbidity. Trefoil proteins protect the gastrointestinal mucosa from damage and aid its repair. TFF2 is considered the major cytoprotective gastric trefoil protein. There is a marked circadian variation in gastric luminal TFF2 in young healthy volunteers with peak levels present during the night. METHODS: Gastric juice was aspirated at two hourly intervals over a 24-h period via a nasogastric tube. TFF2 was measured by quantitative western transfer analysis. Helicobacter pylori (H. pylori) status was measured by C13 urea breath test and by serology. The effects of H. pylori infection, sleep deprivation, and ageing, which cause increased gastric morbidity, on the TFF2 circadian rhythm were tested. RESULTS: H. pylori infection attenuated the increase in TFF2 that occurs during the night. The TFF2 diurnal rhythm was reduced in older people and both the TFF2 level reached and the time at which the maximum TFF2 concentration occurs were associated inversely with age (p < 0.005). Sleep deprivation delayed the normal night time increase in gastric TFF2 and resulted in an overall reduction in TFF2 secretion. CONCLUSIONS: H. pylori infection, ageing, and sleep deprivation cause a reduction in the TFF2 diurnal rhythm. The demonstration that the TFF2 rhythm is impaired in cohorts of individuals known to suffer gastric symptoms suggests that interventions to restore the normal TFF2 rhythm in those with poor mucosal protection could reduce morbidity.

Adolescent↗
PubMed1998

Increased ACTH and corticosterone secretion induced by different methods of paradoxical sleep deprivation.

The methods used to induce paradoxical sleep (PS) deprivation are believed to be stressful. In the present study, two methods were compared in regard to their ability to activate the hypothalamic-pituitary-adrenal (HPA) axis. Animals were placed on multiple large (MLP) or small (MSP) platforms or on single large (SLP) or small (SSP) platforms and blood sampled at the end of a 4-day period of PS deprivation (experiment 1) or on Days 1 (short-term) and 4 (long-term) of PS deprivation (experiment 2). ACTH and corticosterone (CORT) levels were determined by RIA. The results of experiment 1 showed that all experimental animals presented increased ACTH response, compared to controls. CORT levels, however, were only elevated in MSP animals, suggesting increased adrenal sensitivity. Experiment 2 showed that ACTH levels of MSP animals were higher than MLP and SSP animals, and that animals placed on the multiple platform tanks showed the highest ACTH levels on Day 4 of manipulation. CORT levels were elevated in the animals kept over small platforms, and these levels where higher on Day 1 than basal and further elevated on Day 4 of PS deprivation. These results indicate that the multiple platform technique induces a distinct activation of the HPA axis, and that PS deprivation may act as an additional stressor.

Adrenocorticotropic Hormone↗
PubMed1993

Sleep homeostasis in the guinea pig: similar response to sleep deprivation in the light and dark period.

In the guinea pig, sleep and slow-wave activity (SWA) are evenly distributed over 24 h in contrast to the sleep pattern in other rodents where a daily preference for sleep and a decline of SWA within the main sleep period is typical. SWA is regulated as a function of prior waking and is assumed to reflect sleep intensity. We investigated sleep homeostasis and its possible circadian modulation by performing sleep deprivation (SD) at two phases of the light-dark cycle. SD induced an increase in SWA which was similar under both conditions. We conclude that sleep is homeostatically regulated in the guinea pig and is not subject to a circadian modulation.

Animals↗
PubMed2001

[Sleep deprivation as a predictor of response to light therapy in major depression].

Light therapy (LT) is regarded as the treatment of choice for seasonal affective disorder (SAD). In nonseasonal depression the results of light therapy are nonconclusive. Sleep deprivation (SD), however, is effective in 50-60% of the patients with major depression. The predictive value of Total Sleep Deprivation (TSD) for the treatment outcome of antidepressiva has been already examined. Purpose of the present study was to test whether light therapy is more beneficial in TSD responders than in TSD nonresponders. 40 inpatients with major depressive disorder completed one night of TSD. Twenty TSD responders and 20 TSD nonresponders were randomly assigned to 14 days of bright light therapy (2500 lux, 7-9 a.m.) or 14 days of dim light therapy (red light 50 lux, 7-9 a.m.). Manova with repeated measurements revealed a significant difference in the course of depression over the time between TSD responders and nonresponders, but no significant difference between bright and dim light. Questions of placebo effect, of SAD and of personality variables as predictors of response to SD and LT are being discussed.

Adult↗
PubMed2003

Effects of slow-release caffeine and a nap on driving simulator performance after partial sleep deprivation.

A driving simulator was used to evaluate the effectiveness of a 30-min. nap and 300-mg slow-release caffeine as countermeasures to drivers' sleepiness induced by partial sleep deprivation. 12 participants were allowed 45 hr. time in bed at the laboratory. Driving performance then was measured twice--at 9 a.m. and at 1 p.m.--by a 45-min. driving task on a simulator. Subjective sleepiness/alertness and mood were assessed four times on the Stanford Sleepiness Scale and the Profile of Mood States. Driving performance was assessed as Lane Drifting, Speed Deviation, and Accident Liability. A 30-min. nap opportunity and 300 mg of slow-release caffeine both were successful in counteracting drivers' sleepiness. The remedial effect of slow-release caffeine lasted longer than that of the nap, that is, it was also effective in the afternoon session. This suggests that slow-release caffeine represents a valuable countermeasure that, in the case of partial sleep deprivation, is preferred to a nap when sleepiness has to be counteracted for a longer time.

Accidents, Traffic↗
PubMed2006

Geranylgeranylacetone, an inducer of HSP 70, attenuates REM sleep rebound after sleep deprivation.

The effect of pretreatment of geranylgeranylacetone (GGA), an inducer of heat shock protein (HSP) 70, on responses in sleep and core body temperature (Tcore) against sleep deprivation (SD) was examined in rats. After 3 days of GGA or vehicle injection, a 6-h period of SD was performed. During the recovery period, both rapid-eye movement (REM) and non-REM (NREM) sleep were increased in both GGA- and vehicle-injected rats. However, in GGA-injected rats, REM-sleep rebound was significantly suppressed, while NREM-sleep rebound remained unaffected. In addition, the increase of Tcore caused by SD was also attenuated in GGA-injected rats. In the hippocampus, both SD and the GGA pretreatment induced an increase in the expression of HSP70 mRNA, indicating that the SD functions as a stress for hippocampal neurons and that the GGA induces HSP70 expression. The findings suggest that pretreatment with GGA suppresses REM sleep rebound and the response of Tcore against SD.

Animals↗
PubMed1994

REM-sleep propensity accumulates during 2-h REM-sleep deprivation in the rest period in rats.

Two-hour, highly-selective, rest-period, rapid-eye-movement (REM)-sleep deprivation (RD) was performed on rats to characterize the time-course of the homeostatic response to REM-sleep loss. RD caused a dramatic and progressive increase in the frequency of attempts to enter REM sleep, suppressed non-REM sleep EEG delta power, and (in late rest period trials) was followed by a rebound increase in REM-sleep expression.

Animals↗
PubMed1998

Neuroethologic differences in sleep deprivation induced by the single- and multiple-platform methods.

It has been proposed that the multiple-platform method (MP) for desynchronized sleep (DS) deprivation eliminates the stress induced by social isolation and by the restriction of locomotion in the single-platform (SP) method. MP, however, induces a higher increase in plasma corticosterone and ACTH levels than SP. Since deprivation is of heuristic value to identify the functional role of this state of sleep, the objective of the present study was to determine the behavioral differences exhibited by rats during sleep deprivation induced by these two methods. All behavioral patterns exhibited by a group of 7 albino male Wistar rats submitted to 4 days of sleep deprivation by the MP method (15 platforms, spaced 150 mm apart) and by 7 other rats submitted to sleep deprivation by the SP method were recorded in order to elaborate an ethogram. The behavioral patterns were quantitated in 10 replications by naive observers using other groups of 7 rats each submitted to the same deprivation schedule. Each quantification session lasted 35 min and the behavioral patterns presented by each rat over a period of 5 min were counted. The results obtained were: a) rats submitted to the MP method changed platforms at a mean rate of 2.62 +/- 1.17 platforms h-1 animal-1; b) the number of episodes of noninteractive waking patterns for the MP animals was significantly higher than that for SP animals (1077 vs 768); c) additional episodes of waking patterns (26.9 +/- 18.9 episodes/session) were promoted by social interaction in MP animals; d) the cumulative number of sleep episodes observed in the MP test (311) was significantly lower (chi-square test, 1 d.f., P < 0.05) than that observed in the SP test (534); e) rats submitted to the MP test did not show the well-known increase in ambulatory activity observed after the end of the SP test; f) comparison of 6 MP and 6 SP rats showed a significantly shorter latency to the onset of DS in MP rats (7.8 +/- 4.3 and 29.0 +/- 25.0 min, respectively; Student t-test, P < 0.05). We conclude that the social interaction occurring in the MP test generates additional stress since it increases the time of forced wakefulness and reduces the time of rest promoted by synchronized sleep.

Adrenocorticotropic Hormone↗
PubMed1978

Effect of sleep deprivation on response threshold for signal detectability parameter, beta.

In contrast to a previous study (Deaton, Tobias, & Wilkinson, 1971), data are presented which demonstrate significant decreases in response bias (beta) as well as sensitivity (d') following one night of sleep deprivation. It is argued that previous failures to observe significant decreases in beta may be related to the disparity in the number of noise and signal-plus-noise trials in these experiments. The use of parametric analysis to test the effect of sleep deprivation on d' and beta is recommended.

Humans↗
PubMed2002

Influence of sleep deprivation on neuroactive steroids in major depression.

There is evidence from preclinical and clinical studies that concentrations of neuroactive steroids are altered in depression and normalize after antidepressant pharmacotherapy. However, no data are available concerning the impact of sleep deprivation on the concentrations of neuroactive steroids. A total of 29 drug-free patients (12 men, 17 women) suffering from major depression according to DSM-IV criteria were treated with partial sleep deprivation (PSD). Response to PSD was defined as a reduction of at least 30% according to the six-item version of the Hamilton depression scale (6-HAMD). Plasma samples were taken the day before and after PSD (days 0 and 1) and after one night of recovery sleep (day 2) at 8:00 am. The samples were quantified for neuroactive steroids by means of a highly sensitive and specific combined gas chromatography/mass spectrometry analysis. There was no influence of PSD on the concentrations of neuroactive steroids either in PSD responders (n=20) or in nonresponders (n=9). However, nonresponders showed significantly higher concentrations of 3alpha,5alpha-tetrahydroprogesterone (3alpha,5alpha-THP), 3alpha,5beta-tetrahydroprogesterone (3alpha,5beta-THP), and dehydroepiandrosterone (DHEA) before or after PSD compared to responders. In contrast to antidepressant drugs, which correct the dysequilibrium of neuroactive steroids in major depression within several weeks, PSD does not affect the concentrations of neuroactive steroids either in responders or in nonresponders.

Adult↗
PubMed1993

Effect of rapid eye movement sleep deprivation on rat brain Na-K ATPase activity.

Since rapid eye movement (REM) sleep deprivation has been reported to affect the neuronal excitability in the brain, it was hypothesized that a change in the neuronal membrane-bound Na-K ATPase activity might be at least one of the factors inducing such a change. Therefore, in this study rats were deprived of REM sleep by using the platform technique and enzyme activity was estimated in the whole brain, in different regions of the brain and in microsomal preparations. Deprivation was carried out for varying periods and suitable control experiments were conducted to rule out the possibility of nonspecific effects. The observation supported our hypothesis and showed primarily that the deprivation increased the enzyme activity in the rat brain. It showed also that the pons and the medulla were the first sites to be affected by deprivation. The probable mechanism producing such a change is discussed.

Journal Article↗
PubMed1994

Effects of chronic sleep deprivation on central cholinergic receptors in rat brain.

Rats subjected to chronic total sleep deprivation (TSD) by the disk-over-water method have shown very large, sustained rebounds in paradoxical sleep (PS) (also known as REM sleep). Other studies have indicated that cholinergic mechanisms are involved in the instigation and maintenance of PS. Hypothetically, the large PS rebounds could be mediated by an upregulation of cholinergic receptors during TSD. To evaluate this hypothesis, regional brain cholinergic receptors were compared in rats subjected to 10-day TSD by the disk-over-water method (TSD rats), yoked control (TSC) rats which received the same physical stimulation but with much smaller reductions in sleep, and home cage control (HCC) rats. L-[3H]nicotine and [3H]quinuclidinyl benzilate were used as specific cholinergic radioligands for nicotinic and muscarinic receptor binding assays, respectively. Nicotinic receptor binding was not significantly different among groups for any of the brain regions assayed, including frontal cortex, parietal cortex, thalamus, amygdala, hippocampus, anterior hypothalamus, posterior hypothalamus, caudate, limbic system (including septal area, olfactory tubercle, and nucleus accumbens), midbrain, pons, and medulla. Thus, there was no evidence that changes in nicotinic receptors mediate the PS rebounds. For muscarinic receptor binding, TSD rats differed significantly from control rats only in showing a higher binding affinity than TSC rats in the limbic system and a lower binding density than HCC rats in the hippocampus. On the other hand, significant differences in muscarinic receptor binding sites between rats selectively deprived of PS and their yoked controls were found only for the septal area.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1991

Sleep deprivation in the rat: XIV. Comparison of waking hypothalamic and peritoneal temperatures.

Earlier studies of rats subjected to total sleep deprivation (TSD) by the disk-over-water method had shown an initial increase in waking peritoneal temperature (T(ip)) followed by an even greater decrease as deprivation proceeded. In the present study, hypothalamic temperature (T(hy)), as well as T(ip), were recorded continuously. As in the earlier studies, TSD rats showed an increase in energy expenditure and an initial increase followed by a decrease in T(ip). Waking T(hy) showed a more prolonged initial rise and a smaller late decline than waking T(ip) Assuming that, as the literature suggests, T(hy) is held closer to temperature setpoint (TSET) than is T(ip), the present results suggest an elevated waking TSET during deprivation. T(ip) became progressively lower than T(hy) over the course of deprivation, indicating a decreased ability to maintain the whole body near TSET. This decreased ability could result from insufficient thermogenesis or excessive heat loss. Because thermogenesis rose progressively throughout deprivation, heat loss must have increased even more than heat production. Thus, the results are consistent with other data which indicate that TSD in the rat produces two opposing effects on waking temperature, an elevation of setpoint and excessive heat loss, which together increase the demand for energy expenditure.

Animals↗
PubMed1979

Pain thresholds in rats during recovery from REM sleep deprivation.

Using 30 Sprague-Dawley female rats, threshold to pain was measured over the course of recovery from REM sleep deprivation. Relative to the untreated controls and to their own pretreatment thresholds, the REM-deprived animals showed significantly reduced pain thresholds which were still evident 96 hours after the termination of the REM deprivation. Possible implications of these data for research with analgesic drugs were noted.

Animals↗
PubMed1986

REM sleep deprivation facilitates the estrogen effect on heterotypical sexual behavior in male rats.

Gonadectomized male rats were submitted to REM sleep deprivation (REMd) for 120 hr and their hetero and homotypical sexual response to estradiol benzoate (EB) was tested. Subjects (Ss) receiving 20 micrograms EB showed lordosis quotients (LQ) twice as high as those receiving 10 micrograms EB and at the same time the LQs in these groups were higher than in the non-REMd groups. Gonadectomized-adrenalectomized control Ss showed the highest levels of lordosis throughout the experiment. REMd by itself does not produce lordosis response. The results indicate that the brain structures underlying this behavior in males are probably similar to those in females, since REMd increases lordosis in both cases. The lack of homotypical sexual behavior normally observed in gonadectomized male rats does not seem to be affected by this treatment. The issue of adequate controls for REMd experiments is discussed.

Animals↗
PubMed2005

Worsening effect of partial sleep deprivation on indomethacin-induced gastric mucosal damage.

The present study was to investigate the roles of cyclooxygenase-1 and -2 (COX-1 and COX-2) and prostaglandin (PG) on gastric mucosal integrity of partially sleep deprived (PSD) rats. A slowly moving drum was used to induce PSD. The PG levels in the gastric mucosa of PSD rats, with or without indomethacin or rofecoxib treatment, were determined. Exogenous prostaglandin E (PGE) analog, misoprostol, was administered to PSD rats to investigate the modulating effect of PG in indomethacin-induced gastric damage. It was observed that COX-1 mRNA and protein were up-regulated in the gastric mucosa of PSD rats. Selective COX-2 inhibition by rofecoxib failed to decrease mucosal PGE2 levels nor to affect mucosal integrity in both PSD and sleep undisturbed rats. However, indomethacin, a COX-1 preferential non-selective COX inhibitor, significantly reduced mucosal PGE2 content and produced more severe mucosal damage in PSD rats than in the controls. The deleterious effect of indomethacin on gastric mucosal integrity of PSD rats was significantly attenuated with the administration of misoprostol. These results suggest that PSD enhances COX-1 biosynthesis of gastroprotective PGE2 as an adaptive response of the stomach to stress. The administration of non-selective COX inhibitors to subjects with chronic sleep deprivation may induce more gastric damages.

Animals↗
PubMed1996

Serum prolactin, growth hormone, total corticoids, thyroid hormones and thyrotropine during serial therapeutic sleep deprivation.

In 13 patients fulfilling DSM-III-R criteria for a major depressive episode, hormone serum levels were measured at 8 AM on the day before and on the first and second days after partial sleep deprivation (PSD) late in the night during a 4-week course of therapy with amitriptyline in combination with 6 PSDs. Prolactin, human growth hormone (HGH) and total corticoids were not influenced by PSD. In contrast, T3 and thyrotropine (TSH) were elevated significantly on the 1st day after PSD throughout the series, but T4 less regularly. Although TSH reverted regularly to baseline values on the 2nd day after PSD, i.e. after a full night's sleep, T3 remained elevated. The hormones under discussion do not predict the therapeutic PSD effect. Nor can any correlation be determined between endocrine and clinical changes on the 1st or 2nd day after PSD. In connection with findings from sleep deprivation research in animals and in healthy subjects, the results suggest that thyroid changes under PSD may be nonspecific and unrelated to antidepressive PSD effects.

Adrenal Cortex Hormones↗