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Rapid eye movement sleep deprivation for 3 to 4 days by the platform pedestal procedure produced an increase in sexual behaviour of male rats. The possible factors contributing towards the increase in sexual behaviour are discussed.
All night sleep deprivation prior to an EEG registration causes some inconvenience not only to the organization of the EEG department but presents a burden on the patients as well as their family members, and for these reasons is not suitable to be frequently employed as a routine procedure. As an alternative, we performed short-term sleep recordings in the early afternoon following a partial sleep deprivation of the patients during the preceding night. This method was well accepted by the patients and their family. Our only goal was to shorten the total time of night sleep using the following guideline: for very small children 22.00-06.00; for 4-14-year-old patients 24.00-06.00; and for patients older than that 01.00-06.00. 79.9%, out of 719 patients (573) who had been given the above instructions subsequently showed sleep patterns in their EEG. Additionally we had to administer an oral dose of promazine to only 67 patients. However, for the most part, patients showed only light sleep stages: 114 patients only reached sleep stage 1; 323 patients sleep stage 2; 88 patients sleep stage 3; and 48 patients sleep stage 4. As expected, REM sleep was never recorded. Nonetheless, in 32 out of 146 patients who were tired but unable to fall asleep, epileptic patterns could be provoked. In 636 patients, the EEG-recording after sleep reduction was ordered because of a suspected seizure disorder; in the remaining patients it was initiated solely because of sharp components in the routine-EEG. In 341 (53.6%) of the patients with suspected epilepsy, electroencephalographic activity indicative of a seizure disorder was activated. Such epileptic patterns were recorded almost exclusively in stages of waking, 1 and 2. Only in one out of the 124 patients who reached sleep stages 3 and 4 epileptic patterns were not seen until deep sleep was entered. We observed 2/s, 3/s and 6/s spike-and-wave complexes, sharp waves, spikes, polyspikes, groups containing remarkably sharp components and so called sharp vertex grapho-elements. Patients with suspected seizure disorders frequently show grapho-elements which can be interpreted as the expression of a disposition for epilepsy. These sharp vertex elements were evident in 54 out of 719 short term sleep recordings, more often in children than in adults. 49 times they coincided with typical epileptic discharges such as sharp waves, spikes or spike-and-waves in the same recording.
Previous research reported changes in steady-state brain electrical activity during sleep. However, due to the quasi-linear nature of the Direct Current (DC) changes, artifact contamination was a potential confound. The present study was performed to further explore DC potentials and to help establish its validity. Twenty-five male university students (13 control and 12 sleep-deprived; mean age 19 y (range 17-27 y) served as subjects. During wakefulness, subjects were tested every hour while standard EEG activity recordings were made, as well as DC measurement. Split plot analyses of variance (ANOVAs) revealed that changes in DC activity levels differed between the two groups. The control subjects showed the same pattern of decreasing DC observed previously with a return to baseline levels during waking hours. The sleep-deprived subjects showed a smaller decrease in DC level through the night, followed by a rise in DC level that continued until the end of the 24 h study. It was concluded that DC measurement reflects changes in brain state associated with fatigue that are not attributable to artifactual processes.
An abnormal dexamethasone suppression test (DST) result, a sensitive and specific marker for endogenous depression, was found to be associated with an antidepressant response to sleep deprivation in patients who met DSM-III criteria for Major Depressive Episode regardless of whether they met criteria for melancholia or psychotic subtypes of this disorder. These findings support previous reports of an association between an abnormal DST result and antidepressant effects of sleep deprivation in depressed patients. Our results extend the positive association between an abnormal DST result and the antidepressant response to sleep deprivation to include depressed patients who are clinically nonmelancholic during their current episode but who have an abnormal DST result.
Ten young men underwent a sleep deprivation of 48 h which resulted in a 19 percent decrease of beard-hair growth. This effect, reflecting the lowering of protein synthesis during sleep deprivation, was presumably related to hormonal disturbance, namely depression of growth hormone release, decrease of dihydroxytestosterone availability or increase of sympathetic tone and/or corticoids.
Six men and 3 women on each of 4 days received 10 mg of methylphenidate or placebo (2 times a day) at 0800 and 1200 after 8 hr or 0 hr of sleep. Sleep latency was measured by the Multiple Sleep Latency Test (MSLT) at 0930, 1130, 1330, 1530, and 1730. Participants also completed divided-attention and auditory vigilance tasks at 1000 and 1400 and the Profile of Mood States (POMS) and the Addiction Research Center Inventory (ARCI) after the 0930 and 1330 latency tests. The drug increased mean latency on the MSLT in both sleep conditions. Performance only showed drug effects after prior sleep deprivation. On the POMS, the drug increased Vigor and reduced Fatigue and Depression scale scores, primarily after sleep deprivation. The drug increased the ARCI Amphetamine and Morphine-Benzedrine scores only in the basal state. The ARCI Pentobarbital score was increased by sleep deprivation and decreased by the drug.
Replenishment of brain glycogen stores depleted during waking has been suggested to constitute one of the functions of sleep [Benington, J. H. & Heller H. C. (1995) Prog. Neurobiol., 45, 347]. We have tested the hypothesis that the level of expression of enzymes involved in glycogen metabolism could undergo variations throughout the sleep-waking or rest-activity cycle, and after 6 h of 'gentle' total sleep deprivation in mice. Specifically, we determined the variations in mRNAs coding for protein targeting to glycogen (PTG), glycogen synthase and glycogen phosphorylase, all considered as key regulators of glycogen metabolism. Glycogen synthase and glycogen phosphorylase mRNAs exhibited significant variations throughout the light-dark cycle with a maximum at the middle of the light period and a minimum at the middle of the dark period. Following sleep deprivation, a two-fold increase in PTG mRNA and a decrease of mRNAs encoding glycogen synthase and glycogen phosphorylase were observed. These transcriptional events have functional consequences as the activity of glycogen synthase was increased 2.5-fold indicating a stimulating effect of sleep deprivation on glycogen synthesis. These results indicate that (i) expression of genes related to brain glycogen metabolism exhibit variations throughout the sleep-waking or rest-activity cycle and (ii) given the almost selective localization of glycogen to astrocytes, these cells might participate in the regulation of sleep.
Electroencephalogram (EEG) wavelength and amplitude within NREM sleep, paradoxical sleep (PS), and wake were measured by computer in five intact rats and four rats with suprachiasmatic nucleus (SCN) lesions for the first recovery day following 24-h total sleep deprivation (TSD) achieved by keeping them on a rotating cylinder over water. To assess exercise effects, EEG within NREM was also analyzed in four intact rats for 8 h after separate 4-h TSD sessions at low and high rates of cylinder rotation (high rate = 12 times low rate). During recovery from 24-h TSD, EEG changed most dramatically in NREM. The number of slow waves per unit time (1-4 Hz wave incidence) and the amplitude at all wavelengths from 1 to 16 Hz were increased for up to 12 h and then fell below baseline levels for most of the next 12 h. Fast (5-16 Hz) wave incidence changed inversely with slow wave incidence. Wake and PS also showed initially increased amplitude, but shifts in incidence were from slow to fast waves. Relative to baseline, intact and SCN-lesioned rats showed similarly shaped recovery functions, indicating that EEG responses to sleep loss are largely independent of diurnal rhythms. Four-hour TSD at a low rotation rate affected NREM EEG similarly to 24-h TSD, but more mildly. The high rotation rate further increased slow wave incidence during recovery without further increasing slow wave amplitude. The results suggest that both EEG wave incidence and amplitude are responsive to prior wakefulness, but only incidence is responsive to prior exercise.
STUDY OBJECTIVES: To evaluate the effects of a 25-hour sleep-deprivation episode on quantitative waking electroencephalogram (EEG) and subjective alertness in young and middle-aged subjects. DESIGN: A 25-hour constant-routine protocol followed by a daytime recuperative sleep episode. SETTING: Chronobiology laboratory. PARTICIPANTS: Twenty-five normal subjects separated into 2 groups: young (aged 20-39 years) and middle-aged (aged 40-60 years). INTERVENTIONS: None. MEASUREMENTS AND RESULTS: Waking EEGs were recorded every 2 hours and subjective measures of alertness every 30 minutes during the 25-hour sleep-deprivation episode. Overall, results indicated no age-related differences over a 25-hour constant routine in the temporal evolution of subjective alertness and of spectral power in the theta/alpha (4-12 Hz) frequencies of the waking EEG. The middle-aged compared to the young subjects showed a reduced rebound of slow-wave activity in the recovery-sleep episode. While the waking EEG and subjective alertness levels showed strong correlations in both groups, there was no relationship between theta rise during wakefulness and slow-wave activity rebound in the recovery-sleep episode. CONCLUSIONS: These results suggest a dissociation in the middle-aged population between the sensitivity of their alertness level on the one hand and the sensitivity of their sleep on the other to the number of hours of wakefulness. Hence, alertness of young and middle-aged subjects would show the same deterioration with an accumulation of wakefulness (possibly reflecting a similar sleep need), yet the middle-aged subjects would be less able to increase their recuperative sleep intensity following enhanced time awake (reduction in sleep ability).
Loss of sleep may result in memory impairment. However, little is known about the biochemical basis for memory deficits induced by sleep deprivation. Extracellular signal-regulated kinase (ERK) is involved in memory consolidation in different tasks. Phosphorylation of ERK is necessary for its activation and is an important step in mediating neuronal responses to synaptic activities. The aim of the present study was to determine the effects of total sleep deprivation (TSD) on memory and ERK phosphorylation in the brain. Rats were trained in Morris water maze to find a hidden platform (a spatial task) or a visible platform (a nonspatial task) after 6 h TSD or spontaneous sleep. TSD had no effect on spatial learning, but significantly impaired spatial memory tested 24 h after training. Nonspatial learning and memory were not impaired by TSD. Phospho-ERK levels in the hippocampus were significantly reduced after 6 h TSD compared to the controls and returned to the control levels after 2 h recovery sleep. Total ERK1 and ERK2 were slightly increased after 6 h TSD and returned to the control levels after 2 h recovery sleep. These alterations were not observed in the cortex after TSD. Protein phosphotase-1 and mitogen-activated protein kinase phosphatase-2, which dephosphorylates phospho-ERK, were also measured, but they were not altered by TSD. The impairments of both spatial memory and ERK phosphorylation indicate that the hippocampus is vulnerable to sleep loss. These results are consistent with the idea that decreased ERK activation in the hippocampus is involved in sleep deprivation-induced spatial memory impairment.
Paradoxical sleep deprivation (PSD) induces changes in behaviors induced by dopaminergic and cholinergic agonists, including increased aggressive behavior and stereotypy, decreased number of yawns, and shedding of bloody tears in male rats. In female rats, however, very little is known about the relationship between PSD and the effect of these drugs. The present study sought to examine this issue. As in males, PSD in females resulted in increased apomorphine-induced stereotypy, decreased pilocarpine-induced chromodacryorrhea, and hyperthermia. Unlike males, however, no apomorphine-induced aggressiveness or apomorphine- and pilocarpine-induced yawning were observed in PSD females. These findings suggest that female sexual hormones may affect the expression of some behaviors and not the neurotransmission as a whole, because drug-induced behaviors in PSD females were partly similar to those observed in PSD males.
We studied the effect of sleep deprivation (SD) on the amount of somatostatin (SRIF) and growth hormone-releasing hormone (GHRH) mRNA in rat hypothalamic nuclei. According to earlier studies SRIF possibly facilitates REM sleep and GHRH slow-wave sleep. Adult male rats were sleep deprived by the gentle handling method either for 6 h during the first half of the light phase or for 12 h during the dark phase. Undisturbed rats sacrificed at the same time as the SD rats served as controls. After oligonucleotide in situ hybridization the amount of SRIF and GHRH mRNA was measured in brain sections by image analysis and cell count. SD increased the amount of SRIF mRNA in the arcuate nucleus (ARC). In the periventricular nucleus (PE) there was no effect. The amount of GHRH mRNA increased in the paraventricular nucleus (PA) in the 6 h SD group but no effect was detected in ARC. In the periventromedial hypothalamic area (pVMH) the amount of GHRH mRNA was higher in the control rats sacrificed in the morning (09.00 hours) than in the afternoon (15.00 hours), and SD had no effect. We conclude that SRIF cells in ARC and GHRH cells in PA are modulated by sleep loss, which is in accordance with the possible sleep regulatory function of these neuropeptides.
In view of the fact that paradoxical sleep deprivation (PSD) modifies cocaine-induced genital reflexes (penile erection [PE] and ejaculation [EJ]), the aim of this study was to address the interaction of cholinergic agents with the action of cocaine on the genital reflexes of PSD male rats. After a 4-day period of PSD, each group was administered with cholinergic drugs 1 h prior to cocaine and was placed in observation cages. The administration of nicotine (0.12, 0.25, 0.5 and 1 mg/kg sc) reduced the frequency and number of animals displaying PE and increased PE latency. Pretreatment with mecamylamine (1.25, 5, 10 and 20 mg/kg sc) also significantly reduced PE frequency for all doses used. The percentage of rats showing EJ was significantly reduced in the group pretreated with 1 mg/kg of nicotine compared with the saline group. The administration of pilocarpine (1.25, 2.5, 5 and 10 mg/kg sc) and atropine (1.25, 5, 10 and 20 mg/kg sc) led to a reduction in the frequency of PE displayed by the rats. These data show that agonist and antagonist cholinergic drugs inhibit genital reflexes in PSD male rats injected with cocaine. The data also suggest that the stimulating action of cocaine in potentiating the sexual effects in PSD rats does not override the effects of the cholinergic mechanisms of sexual behavior.
Electroencephalographic (EEG) studies have shown that corticotropin-releasing factor (CRF) administration induces EEG activation, decreases sleep time both in rats and humans and modifies the sleep pattern in sleep deprived rats. In the present study we have investigated whether CRF neuronal activity could be altered in a situation of disrupted sleep-wake cycle. Sleep deprivation (SD) was induced by keeping the rat for 72 h on a small platform (7 cm) surrounded by water. Immediately after the SD period rats were killed and CRF levels and CRF receptor binding were evaluated in different brain areas. A marked increase in CRF levels was present in the striatum (+224%), limbic areas (+144%) and pituitary (+42%) whereas the hypothalamic CRF content was reduced (-57%). A significant decrease in CRF binding was found in the striatum (-33%) and pituitary (-38%) of sleep deprived rats. These results indicate that CRF neuronal activity is stimulated by SD, suggesting that CRF might play an important role in the physiological regulation of the sleep-wake cycle and that an altered CRF neuronal activity might be involved in behavioral modifications related to sleep disturbances.
RNA and protein contents in glial and neuronal cells of nucleus raphé dorsalis (NRD) increased by 23 and 31%, resp., following the 24-hr sleep deprivation; within 48 hrs the RNA content attained the normal level, the protein content being lower than normal by 21%. In neurons of nucleus raphé pontis (NRP) the macromolecules contents per cell remained unaltered at the first period of the sleep deprivation and elevated by 30% by the end of the second period. Metabolic changes in gliocytes were parallel to this. The findings suggest exhaustion of functional abilities of the NRD neurons in sleep deprivation as opposed to the NRP neurons.
Medical training in the United States often takes the form of a grueling endurance test in which patients are often those most at risk. This Article discusses sleep deprivation among resident physicians in the United States with an eye towards resolving the problem through legal channels. It analyzes the effects of sleep deprivation on resident physicians, with subsequent discussion of the implications for patient care and medical training. Next, it makes comparisons to medical training in other developed nations, as well as regulations that exist in the airline and trucking industries, where public safety is a principal concern. Furthermore, this Article discusses proposals to mend the dilemmas created by sleep-deprived resident physicians through statutory and regulatory reform, deterrence by way of tort law, and unionization or collective bargaining.
Studies conducted on a group of 38 patients with endogenous depression demonstrated that a reaction to sleep-deprivation presenting as improved well-being has a significant predictive potential for treatment with imipramine. Patients who displayed the reaction also significantly more frequently displayed improvement of clinical course (remission; good response). Risk of switching from depression to mania also increased among these patients. Patients responding to sleep-deprivation with improved well-being belonged mainly to the bipolar affective disorder. Neither clinical manifestations of depression, nor the number of relapses, nor the duration period of the disorder, nor basic demographic patterns did show distinct features; nor did they differ significantly from patients who did not respond to sleep-deprivation with improved well-being.
Twenty-four military cadets went through a 5-day period of heavy physical exercise (35% of max O2 uptake), severe calorie supply deficiency (about 36,000 kJ/24 h), and sleep deprivation (2 h of sleep as a total during 5 days). Some cadets compensated for the caloric deficiency, whereas others partly compensated for the sleep deprivation. Fasting and meal- and glucose-induced changes in the plasma concentration of vasoactive intestinal polypeptide (VIP) were measured on separate days during the course and 8 h after the course was finished (day 6). Fasting plasma concentration of VIP increased two- to five-fold during the course, with the highest increase on day 2. The calorie-compensated subjects showed a smaller increase than those who did not receive any calorie or sleep compensation. Intake of a meal or glucose solution lowered the VIP concentration in plasma within 30-60 min to the concentrations found in the control experiments performed several weeks after the course. The results indicate a role of VIP as 'a polypeptide of substrate need'.