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PubMed1992

Sleep deprivation in the rat: XV. Ambient temperature choice in paradoxical sleep-deprived rats.

Previous studies of total sleep deprivation (TSD) and paradoxical sleep deprivation (PSD) in the rat by the disk-over-water method have indicated that both produce changes in thermoregulation. In both kinds of deprivation, there was a progressive, large increase in heat production as indicated by measures of energy expenditure (EE). In TSD there was an initial increase in waking body temperature (Tb) followed by a later decrease; in PSD there was only a progressive decrease. The increases in heat production far in excess of heat storage indicated increased heat loss in both groups. Because the increase in Tb in TSD rats was supported by ambient temperature choices (Tch) in a thermal gradient that became progressively higher during deprivation, an increase in waking temperature setpoint (TSET) was indicated. Because the rats resorted to behavioral warming in spite of greatly increased thermogenesis, they must have had some failure to retain body heat. Prior to the present study, changes in TSET, had not been evaluated in PSD rats. Because they had not shown increases in Tb, PSD rats might not have an elevated TSET, which would indicate a functional difference between PS and nonrapid eye movement (NREM) sleep. Also, an evaluation of behavioral thermoregulation in PSD rats would clarify whether their Tb decline resulted from excessive heat loss or from a lowered TSET. To evaluate changes in heat flow and TSET, EE, Tb and Tch were measured in five PSD rats and their yoked control (PSC) rats. PSD rats showed progressive increases in EE and decreases in Tb as in the earlier PSD study; Tch rose progressively. PSC rats showed minimal changes in all three parameters.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1990

Sleep deprivation in the rat: XI. The effect of guanethidine-induced sympathetic blockade on the sleep deprivation syndrome.

In earlier studies, rats totally deprived of sleep by a disk-over-water apparatus (TSD rats) had shown an increase in energy expenditure (EE) that could not be explained by increased motor activity or the metabolic expense of wakefulness. Excessive activation of a calorigenic mediator was a possibility, and norepinephrine-mediated sympathetic activation was the most likely candidate, because plasma norepinephrine (NE) levels had risen sharply in TSD rats. To determine whether this activation was necessary for increased EE in sleep deprived rats, the peripheral sympathetic blocking agent guanethidine (GU) was administered to six sleep-deprived (GD) rats and their yoked control (GC) rats. GU attenuated the increase in NE previously seen in TSD rats, but the increase in EE was not attenuated. Apparently, NE-mediated sympathetic activation was not critical for increased EE in sleep-deprived rats. On the other hand, plasma epinephrine (EPI) levels were significantly increased in GD (but not in GC) rats above those previously seen in TSD rats, suggesting the substitution of one calorigenic mediator for another in response to an abnormally elevated need for EE. Temperature data suggest that increased need for EE could arise from an elevated temperature setpoint and an inability to retain body heat. GD (but not GC) rats also showed other effects previously seen in TSD rats, including debilitated appearance; severe ulcerative and hyperkeratotic lesions on the tails and plantar surfaces; initially increased and later decreased body temperature; decreased plasma thyroxine; increased triiodothyronine-thyroxine ratio; and eventual death. Evidently, NE-mediated sympathetic activation was not critical to any of these effects, although a role for catecholamines cannot be ruled out.

Animals↗
PubMed1980

[Concentration of proteins and RNA in neurons and gliocytes of the rat locus coeruleus during natural sleep and REM-sleep deprivation].

Natural sleep entails an increase of the RNA concentration and absolute content (per 1 cell) in the gliocytes of the locus coeruleus and a decrease of the protein absolute content in the neuron cytoplasm. Within 24-hr REM-sleep deprivation, the protein and RNA concentrations remained constant in neurons and gliocytes whereas the RNA absolute content decreased in neurons; the 48-hr REM-sleep deprivation increased the protein concentration in neurons and glia (exceeding the wakefulness control values); protein absolute content in gliocytes increased as well, RNA concentration and absolute content remained equal to the control in neurons and in glia. In these respects the locus coeruleus differs from the supraoptic and red nucleus studied previously under the same conditions.

Animals↗
PubMed2000

White blood cells and cortisol after sleep deprivation and recovery sleep in humans.

Sleep deprivation (SD) has enriched our treatment programme for major depression. SD has been demonstrated to modify different host defence activities. There is some evidence that there are reciprocal relationships between immune function and increased hypothalamic-pituitary-adrenocortical (HPA) axis activity in depression. We therefore investigated the number of leukocytes, granulocytes, monocytes, lymphocytes, B cells, T cells, helper T cells, cytotoxic T cells, NK cells and salivary cortisol in 10 healthy men before and after total SD (TSD) as well as after recovery sleep. Blood samples were drawn on 3 consecutive days at 7 am, 1 pm and 7 pm, respectively. Comparison of the 7 am values by contrast analysis yielded significant differences for granulocytes (p = 0.044) and NK cells (p = 0.001) after SD and recovery sleep. NK cells decreased and granulocytes increased after SD and after recovery sleep. Significant differences between single points in time across the day were found for granulocytes (p = 0.022), monocytes (p = 0.031), T cells (p = 0.005), helper T cells (p = 0.004), cytotoxic T cells (p = 0.005) and NK cells (p = 0.017). No significant difference could be detected for leukocytes, lymphocytes and B cells counts. These results favour the thesis that SD and recovery sleep lead to changes in the distribution of peripheral leukocytes, especially in a reduction of NK cells after SD and recovery sleep. The cortisol rhythm was affected neither by SD nor recovery sleep.

Adult↗
PubMed1993

Dopamine and opioids interactions in sleep deprivation.

1. Sleep deprivation induced by the platform technique is considered to be a heavy stressful situation in rats. At the end of the sleep deprivation period (72 hrs) the rat displayed particular behavior characterized by wakefulness, a high degree of motor and exploratory activity, increased alertness and reactivity to environmental stimuli. 2. Our results indicate that this behavior is potently antagonized by the administration of D1 antagonist SCH 23390 and by the opioid antagonist naloxone. 3. We also show that concomitantly to this behavior, an increased number of D1 receptors associated with an increased dopamine-stimulated adenylate cyclase activity is present in the limbic system but not in the striatum of these animals. On the contrary, a decreased Bmax of mu and delta opioid receptors was found in the same brain areas. 4. These data suggest an active role of limbic dopamine and opioid system in the generation of arousal and insomnia related to sleep deprivation-induced stress.

Adenylyl Cyclases↗
PubMed1992

Dopamine D1 and opioid receptor binding changes in the limbic system of sleep deprived rats.

Sleep deprivation induced by the platform technique is considered to be a heavy stressful situation in rats. At the end of the sleep deprivation period (72 h) the rat displayed particular behavior characterized by wakefulness, a high degree of motor and exploratory activity, increased alertness and reactivity to environmental stimuli. Our previous results indicated that this behavior was potently antagonized by the administration of the D1 selective antagonist SCH 23390 and by the opioid antagonist naloxone. In this paper we show that concomitantly to this behavior, an increased number of D1 receptors associated with an increased dopamine-stimulated adenylate cyclase activity is present in the limbic system but not in the striatum of these animals. On the contrary, a decreased Bmax of mu and delta opioid receptors was found in the same brain area. These data suggest an active role of limbic dopamine and opioid systems in the generation of arousal and insomnia related to sleep deprivation-induced stress.

Animals↗
PubMed2000

Vocalization thresholds related to noxious paw pressure are decreased by paradoxical sleep deprivation and increased after sleep recovery in rat.

The aim of this study was to assess the effect of paradoxical sleep deprivation (PSD) and sleep recovery on the vocalization threshold in rats submitted to a mechanical noxious stimulus. Sixteen male Wistar rats were randomly assigned in two groups: controls (n=8), paradoxical sleep deprived rats (n=8). PSD was performed using the 'inverted flower pot' technique. Paw pressure test was used to assess the sensitivity to mechanical noxious stimulus (vocalization threshold). The experiment was divided into three periods: baseline (day 1, day 2), PSD (day 3, day 4, day 5) and recovery (day 6, day 7, day 8, day 9). After 48 and 72 h of PSD, the vocalization thresholds decreased significantly in comparison to the control rats (day 4: 245+/-21 vs. 303+/-20 g, P=0.05; day 5: 256+/-17 vs. 324+/-22 g, P=0.02). In PSD group, relative to controls, vocalization thresholds increased significantly after 48, 72, and 96 h of recovery sleep periods (day 7: 378+/-24 vs. 307+/-8 g P=0.01; day 8: 384+/-27 vs. 316+/-23 g, P=0.02; day 9: 395+/-24 vs. 328+/-15 g, P=0.02). Vocalization thresholds on day 6 were not significantly different in both groups (375+/-20 vs. 324+/-24 g, P=0.08). In conclusion, experimental PSD in rats induces a significant decrease in vocalization threshold to mechanical noxious stimulus, which is totally reversed during the sleep recovery period.

Animals↗
PubMed1996

Bright light therapy stabilizes the antidepressant effect of partial sleep deprivation.

Partial sleep deprivation (PSD) results in a pronounced decrease of depressive symptoms in the majority of patients with major depressive disorder. Generally this acute antidepressant effect is not stable, relapse usually occurs after one night of recovery sleep. We therefore studied whether light therapy, beginning in the morning after PSD, is able to prevent the relapse after sleep deprivation, using a controlled, balanced, parallel design. All patients received an antidepressant medication, which was kept constant before and during the study period. Fourteen of 20 patients (70%) showed a reduction of at least 40% in the Hamilton Depression Rating Scale (HDRS) in the morning after PSD and were classified as PSD responders. Responders as well as nonresponders were randomly assigned to receive either bright light (BL/3000 lux) or dim light (DL/100 lux) therapy during the following 6 days after PSD. In the responder group BL therapy prevented significantly (p = 0.005) the relapse after the next night of sleep and prolonged significantly (p = 0.011) the antidepressant effects of PSD up to 7 days. In contrast, patients in the DL condition relapsed after the recovery night and showed no further improvement of the depressive syndrome after 1 week of DL therapy. PSD nonresponders did not benefit from light treatment. These findings indicate that BL therapy might be efficacious to prevent relapse after PSD.

Adult↗
PubMed2003

Human sleep spindle characteristics after sleep deprivation.

OBJECTIVE: Sleep spindles (12-15 Hz oscillations) are one of the hallmarks of the electroencephalogram (EEG) during human non-rapid eye movement (non-REM) sleep. The effect of a 40 h sleep deprivation (SD) on spindle characteristics along the antero-posterior axis was investigated. METHODS: EEGs during non-REM sleep in healthy young volunteers were analyzed with a new method for instantaneous spectral analysis, based on the fast time frequency transform (FTFT), which yields high-resolution spindle parameters in the combined time and frequency domain. RESULTS: FTFT revealed that after SD, mean spindle amplitude was enhanced, while spindle density was reduced. The reduction in spindle density was most prominent in the frontal derivation (Fz), while spindle amplitude was increased in all derivations except in Fz. Mean spindle frequency and its variability within a spindle were reduced after SD. When analyzed per 0.25 Hz frequency bin, amplitude was increased in the lower spindle frequency range (12-13.75 Hz), whereas density was reduced in the high spindle frequency range (13.5-14.75 Hz). CONCLUSIONS: The observed reduction in spindle density after SD confirms the inverse homeostatic relationship between sleep spindles and slow waves whereas the increase in spindle amplitude and the reduction in intra-spindle frequency variability support the hypothesis of a higher level of synchronization in thalamocortical cells when homeostatic sleep pressure is enhanced.

Adult↗
PubMed1978

Changes in sleep pattern after sleep deprivation.

Total sleep deprivation (TSD) was performed for one night with 11 healthy male students and three-consecutive-recovery night-sleep was recorded. Special attention was paid to the analysis of the individual difference in SWS(min, %) on the baseline and recovery nights. The total sleep time increased on the first recovery night compared to the baseline, but it decreased significantly on the second and third recovery nights. Stage 1(%) decreased significantly on the first and second recovery nights. Stage SWS(min) showed a significant increase on the first recovery night, while SWS(%) increased significantly on the first and second recovery nights. As for Stage REM(%), there was no significant difference between the baseline and the recovery nights. There was a positive correlation between SWS(min) on the baseline and that on the recovery nights. SWS(%) also showed the same results as those obtained with SWS(min). Between SWS(min) in the baseline and the increase rate of SWS(min) on the first recovery night, there was a significant inverse correlation, while there was a tendency to inverse correlation on the second and third recovery nights. As to SWS(%), there was a significant inverse correlation between SWS(%) in the baseline and the increase rate of SWS(%) on the first and third recovery nights.

Adult↗
PubMed1976

Effects of selective sleep deprivation on sleep-linked prolactin and growth hormone secretion.

1. The secretion of prolactin and growth-hormone (hGH) was investigated during sleep in 10 healthy volunteers (8 males and 2 females): The comparison of one baseline night, one night after daytime physical exercise, and one night with selective deprivation of sleep stages 3 and 4 and paradoxical sleep showed clear differences of prolactin and hGH secretion during sleep. 2. Prolactin secretion is entrained into the sleep cycle of Non-REM and REM periods. A maximum of plasma hormone elevations occurs during the first quarter of sleep cycles, i.e., during Non-REM periods and less frequent rises at the end of the cycles, mainly during REM periods. 3. In contrast to growth hormone, concentrations of prolactin remain high also during later cycles occurring toward morning. This shows that high prolactin, but not high concentrations of hGH, regularly occur during sleep cycles with small amounts of slow-wave sleep. 4. Maximal prolactin concentrations during sleep are affected neither by preceding daytime physical exercise nor by selective deprivation of slow sleep stages 3 and 4. This is further evidence that slow-wave sleep stages are not necessary for the development of high plasma prolactin concentrations. However, peak values of growth hormone in the first and second cycle are significantly diminished after selective deprivation of sleep stages 3 and 4. 5. In abnormally long sleep cycles with artificial delay of the first REM period, the cyclical rhythmicity of prolactin release seems disturbed. This is further evidence for the sleep-dependent rhythmicity in the secretion of this hormone.

Adult↗
PubMed1990

Sleep reduction in night-shift workers: is it sleep deprivation or a sleep disturbance disorder?

Two explanations of the reported reduction in night-shift workers' sleep length have emerged. One argues that these reductions in sleep are related to sleep disturbances which may require medical treatment as disorders. The other argues that sleep reduction is mainly due to a sleep deficit caused by the voluntary choice to delay sleep onset and reduce the sleep duration which requires a systems approach aimed at increasing sleep length and reducing the effect of a sleep deficit at the workplace. Using survey data from 1078 industrial shift workers, this study demonstrates that permanent night workers reporting sleep difficulties, as well as those who do not, report sleep reductions. This finding is interpreted as supporting, in part, the position that night-shift workers suffer primarily from a self-induced sleep deficit.

Adolescent↗
PubMed1999

How to preserve the antidepressive effect of sleep deprivation: A comparison of sleep phase advance and sleep phase delay.

Total sleep deprivation (TSD) leads to an immediate amelioration of depressed mood in approximately 70 % of patients with the melancholic subtype of depression. The clinical utility of this procedure is limited, as the improvement usually subsides after the next night of sleep. In the present study, 40 depressed inpatients, being free of psychoactive medication for at least 7 days and who had responded to a TSD were then distributed (according to a matched-pair design) to a sleep phase advance (SPA = time in bed scheduled from 1700-2400 hrs) or a sleep phase delay (SPD = time in bed from 0200-0700 hrs) with a succeeding shift back (for one hour in the SPA group per day) respectively shift forward (for 30 minutes in the SPD group per day), until the initial sleep phase (2300-0600 hrs) was reached after seven days again. Based on previous observations it was hypothesized that a phase advance of the sleep period should prevent responders to TSD from relapsing. Whereas 75% of the TSD responders were stabilized by the phase advanced condition and did not relapse over a period of seven days, only 40% of the patients in the phase delayed condition did not relapse. Polysomnography during the course of the study gave no evidence that the unusual sleep schedules caused prolonged sleep deprivation. Abnormalities of REM sleep persisted both in the clinical responders and non-responders after the sleep wake manipulation. It is concluded that the clinical effectiveness of TSD can be significantly improved by combining TSD with a following phase advance of the sleep period.

Adult↗
PubMed1985

Platform sleep deprivation affects deep slow wave sleep in addition to REM sleep.

Rats were sleep deprived by the platform method to look for differential effects on light and deep slow wave sleep depending on platform size. Diameters of large and small platforms were 15 cm and 5.1 cm respectively. Sleep was recorded during a baseline light period (09.00-19.00 h), continuously during 48 h of sleep deprivation and during the first lights on recovery period (09.00-19.00 h). In both platform conditions REM sleep was virtually abolished during the first light period (hours 0-10 of sleep deprivation), while NREM sleep was reduced to approximately half of control values. During the second light period (hours 22-34 of sleep deprivation) REM sleep recovered somewhat in the large platform group. Light slow wave sleep (SWS-1) was comparable to baseline while deep slow wave sleep (SWS-2) was still significantly reduced. In the small platform group both SWS-2 and REM sleep was considerably reduced on day 2. Over the whole deprivation period there was an effect of platform size on SWS-1 (higher in the small platform group), and on SWS-2 and REM sleep (lower in the small platform group). During the 9 h light-time recovery sleep there was an REM sleep rebound in both groups. SWS-1 was reduced in both groups while SWS-2 was not significantly increased. The ratio SWS-2/SWS-1 was, however, significantly increased only in the small platform group recovery sleep. The results suggest that platform sleep deprivation deprives the animals of deep slow wave sleep in addition to REM sleep. This has implications for conclusions on REM sleep function based upon REM sleep deprivation.

Animals↗
PubMed1985

Effect of midazolam and sleep deprivation on day-time sleep propensity.

The combined effect of midazolam (Ro 21-3981, Dormicum) and sleep deprivation on day-time sleep propensity was investigated in young, healthy adults. The oral administration of midazolam (15 mg) or placebo at bedtime was followed either by a sleep period of 7 or 4 h, or by no sleep at all. Sleep propensity was recorded at 2-h intervals throughout the following day by the multiple sleep latency test and self-ratings of tiredness. Performance was assessed in the morning and afternoon by a psychomotor test. Partial and total sleep deprivation caused a marked and significant increase of day-time sleep propensity. However, there was no significant difference between the midazolam and placebo condition after 7 or 4 h of sleep. After total sleep deprivation, sleep propensity was higher after placebo than after midazolam. Neither the treatment nor sleep duration had a significant effect on performance. The results show that a bedtime dose of 15 mg midazolam followed by normal or restricted sleep does not significantly affect day-time alertness.

Adult↗
PubMed2006

A reassessment of the hyperphagia/weight-loss paradox during sleep deprivation.

STUDY OBJECTIVES: Sleep deprivation is a well-known paradigm to investigate the deleterious effects of prolonged wakefulness. Previous studies have shown that, during sleep deprivation, rats are hyperphagic but, paradoxically, lose body weight. This phenomenon has been attributed to increased metabolism. However, most previous studies have failed to account for food spillage, which may be considerable during sleep deprivation. DESIGN: In the present study, we revisited the issue of feeding changes in sleep-deprived rats and introduced different procedures to allow accurate estimation of food spillage prior to, during, and after 120 hours of sleep deprivation by a single platform technique. SETTING: Animal Sleep Research Laboratory, Psychobiology Department, Universidade Federal de São Paulo, Brazil. MEASUREMENTS AND RESULTS: The main finding was that, once corrected for spillage, food intake was not significantly increased during sleep deprivation. Increases in food removed from feeders were accompanied by proportional increases in food spillage, resulting in no net changes in food intake. Further, weight loss did occur during the sleep-deprivation period, especially in the first 24 hours, and it was actually explained by a reduction in food intake. CONCLUSION: The hyperphagia/weight-loss paradox previously seen during prolonged sleep deprivation does not necessarily occur with shorter periods of deprivation. Although we found no evidence of hyperphagia for up to 5 days of sleep deprivation in chow-fed rats, our data suggest that an impairment in the ability to increase food intake in response to increased energy expenditure contributes to the energy deficit during sleep deprivation in rats.

Animals↗
PubMed2004

Hormone treatment facilitates penile erection in castrated rats after sleep deprivation and cocaine.

Sleep deprivation is associated with cocaine-enhanced genital reflexes in male rats, and castration of the male rat causes a decline in sexual behaviour, which can be reversed by hormone administration. We conducted two experiments to determine whether sleep deprivation and cocaine administration could also induce spontaneous penile erection in castrated rats after hormonal treatment (testosterone, progesterone and oestradiol). Different doses of hormones or vehicle were administered to rats during the 4-day period of sleep deprivation, and in home-cage control rats. Testosterone did not restore penile erection in castrated sleep-deprived rats. Progesterone triggered penile erection, and 100 mg/day of progesterone induced the highest proportion of rats displaying penile erection, and restored the frequency of penile erection observed in noncastrated sleep deprived rats. Penile erection was absent in vehicle as well as oestradiol-treated sleep-deprived castrated rats. Whereas sleep deprivation increased progesterone concentrations in noncastrated rats, sleep deprivation decreased progesterone concentrations in castrated rats. Corticosterone concentrations were lower in the castrated sleep-deprived rats than in respective control group. These data show that progesterone treatment facilitates penile erection in sleep deprived-cocaine castrated rats.

Animals↗