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A Rechtschaffen

Publications and source records attributed to A Rechtschaffen.

At least 55 records · Page 3Linked to original sources

Sleep deprivation in the rat: X. Integration and discussion of the findings.

The results of a series of studies on total and selective sleep deprivation in the rat are integrated and discussed. These studies showed that total sleep deprivation, paradoxical sleep deprivation, and disruption and/or deprivation of non-rapid eye movement (NREM) sleep produced a reliable syndrome that included death, debilitated appearance, skin lesions, increased food intake, weight loss, increased energy expenditure, decreased body temperature during the late stages of deprivation, increased plasma norepinephrine, and decreased plasma thyroxine. The significance of this syndrome for the function of sleep is not entirely clear, but several changes suggested that sleep may be necessary for effective thermoregulation.

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NREM sleep with low-voltage EEG in the rat.

NREM sleep in the rat has traditionally been defined by electroencephalographic (EEG) amplitudes above those of wakefulness (W) and paradoxical sleep (PS); we refer to this high-amplitude NREM sleep as "HS." We have found that approximately 5% of total time is occupied by episodes in which EEG amplitude is low, distinguishing it from HS; theta amplitude is low, distinguishing it from PS; and electromyographic (EMG) amplitude is low, distinguishing it from W. We have called these low-EEG, low-theta, low-EMG episodes "low-amplitude sleep" (LS). Three studies are done to elucidate additional characteristics of LS. Polygraphically scored 30-s epochs were matched with independent classifications of rat behavior as W, NREM, or PS; 87% of polygraphically scored LS epochs were matched with NREM sleep behavior. Response thresholds to noxious stimuli were lowest in W, intermediate and similar in LS and HS, and highest in PS. The incidence of PGO-type (ponto-geniculo-occipital) waves in W, HS, and LS were all very low in comparison with rates in PS. Thus, LS and HS exhibited similarly quiescent spontaneous behavior, similar intermediate response thresholds, and similar low rates of PGO-type activity. Accordingly, we have proposed that LS, along with HS, is an NREM sleep stage.

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Period-amplitude analysis of rat electroencephalogram: effects of sleep deprivation and exercise.

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.

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Period-amplitude analysis of rat electroencephalogram: stage and diurnal variations and effects of suprachiasmatic nuclei lesions.

Period-amplitude analysis was used to measure the number of waves per unit time (wave incidence) and wave amplitude for 19 wavelength categories in the lateral cortical electroencephalogram (EEG) of five intact and four suprachiasmatic nuclei-lesioned rats during NREM sleep, waking, and paradoxical sleep (PS) over a period of 24 h. The analysis confirmed several parallels between rat electroencephalogram (EEG) and human EEG: The wave incidence and amplitude at all wavelengths are both practically indistinguishable between wake, PS, and NREM sleep onset. As NREM sleep EEG amplitude increases, slow wave incidence and amplitude increase. The incidence and amplitude of slow waves are greatest at the start of the diurnal NREM sleep period and lowest at its end. The pattern of diurnal variation of the NREM EEG may be modeled using two wave generators (sources of variation), one between 1 and 4 Hz, and the other between 5 and 16 Hz. The diurnal patterns for wake and PS are less clear, but both appear to require three generators, one below 3 Hz, one between 3.5 and 6 Hz, and one above 9 Hz. The EEG of suprachiasmatic nuclei-lesioned rats does not show any shift to longer wavelengths in NREM sleep. Wake, PS, and NREM EEG in these rats have a lower incidence and amplitude of slow waves than the corresponding stages in intact rats. One explanation is an inhibition of the slow wave generator as a result of the lesions.

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Strain differences in the sleep of rats.

Sleep was measured in two inbred rat strains (Lewis and Brown Norway) and their F1 hybrids to investigate patterns of inheritance and to provide a starting point for future studies of F2 and recombinant rats. Recordings from chronically implanted electrodes were quantified and scored by a computerized system; results were evaluated by an analysis of variance with pairwise comparisons by the Tukey HSD test. Brown Norway rats had the highest paradoxical sleep (PS) percentages; Lewis rats had the lowest. Hybrid rats had PS percentages intermediate between parent strains and significantly different from both. These results suggest codominance or multigenic transmission of PS amounts. There were no group differences of number of PS bouts; Brown Norway and hybrid rats had longer bouts than Lewis rats. Lewis and hybrid rats had similar amplitudes of the diurnal rhythm of PS, which were higher than those of Brown Norway rats; single gene transmission remains possible for diurnal rhythm amplitude. Thus, inheritance of PS percentage and rhythm amplitude appear independent. No group differences in PS latency were found.

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Relationships among wake episode lengths, contiguous sleep episode lengths, and electroencephalographic delta waves in rats with suprachiasmatic nuclei lesions.

The lengths of sleep and wake episodes during 2 consecutive days of recording were measured in five rats lacking circadian rhythms owing to lesions of the suprachiasmatic nuclei. Total sleep (TS) episode lengths and the amount of NREM sleep and paradoxical sleep (PS) within each episode were examined in relationship to the lengths of the immediately preceding and the immediately following wake episodes. As putative measures of sleep intensity, average and maximum delta wave (1-4 Hz) incidence and amplitude within NREM were also examined in relation to adjacent wake episode lengths. For sleep episodes longer than 50 min (78% of daily sleep), TS episode lengths and amount of NREM within these episodes showed significant positive correlations with both prior and subsequent wake episode lengths. PS durations within sleep episodes also showed significant positive correlations with subsequent wake episode lengths, but little correlation with prior wake episode lengths. The results suggest that in the absence of sleep-wake circadian rhythms, sleep time is subject to short-term homeostatic regulation. Amounts of PS within sleep episodes were highly correlated (r = 0.84) with amounts of NREM. NREM delta wave incidence and amplitude showed no significant relationships with the lengths of prior or subsequent wake episodes, suggesting that variations in sleep intensity may not play a prominent role in the short-term homeostatic regulation of ad lib sleep. Delta wave incidence and amplitude were also not correlated with the duration of NREM episodes, but incidence during wake was positively correlated with wake episode duration, suggesting that delta density during wake may be an electrophysiological indicator of the propensity to sleep.

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Periodic water availability is not a potent zeitgeber for entrainment of circadian locomotor rhythms in rats.

Entrainment of tilt-cage measured circadian activity rhythms to a 2 hr daily period of water availability was assessed in rats fed either an oil-chow mash, which rats readily consume in the absence of water, or dry pellet chow, which rats less readily consume in the absence of water. Four of 6 pellet fed rats but only 2 of 14 mash fed rats exhibited entrainment to water access. Periodic water availability, unlike periodic food availability, thus does not appear to be a potent zeitgeber for circadian activity rhythms in the rat. The entrainment that does occur in some rats may result from shifting of food intake to coincide with the availability of water.

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Recovery of anticipatory activity to restricted feeding in rats with ventromedial hypothalamic lesions.

Entrainment of circadian activity rhythms to a fixed daily mealtime was measured in intact and ventromedial hypothalamic (VMH) lesioned rats housed in tilt-cages. Intact rats showed a clear increase in activity for 2-3 hr prior to the 2 hr daytime feeding period. Anticipatory activity in lesioned rats was attenuated or absent during restricted feeding 5-9 weeks after surgery, but was evident in all rats, even those bearing apparently total VMH damage, during a second restricted feeding schedule 14-21 weeks after surgery. These results show recovery of function and argue against a necessary role for the VMH in food entrained rhythms.

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Suprachiasmatic nuclei lesions eliminate circadian temperature and sleep rhythms in the rat.

We conducted a long-term study of the circadian rhythms of temperature and sleep in the rat after lesions of the suprachiasmatic nuclei (SCN). Brain temperature was measured with thermistors and sleep-wake was scored on the basis of continuously recorded EEG using a computerized system. Rats with complete SCN lesions did not exhibit circadian rhythms in constant dim illumination. Rats with partial SCN lesions generated weak and variable free-running rhythms, and when exposed to a light-dark cycle, some showed a reduced amplitude and altered waveform relative to normal rats. A few rats with partial SCN lesions showed a recovery of function. There was little difference between the circadian rhythms in temperature and waking, and these measures responded similarly to all lesions. Thus, no support was found for the notions that anatomically distinct oscillators control the circadian rhythms of temperature and activity, or that an oscillator outside of the SCN controls the circadian rhythm of temperature.

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Physiological correlates of prolonged sleep deprivation in rats.

The issue of whether sleep is physiologically necessary has been unresolved because experiments that reported deleterious effects of sleep deprivation did not control for the stimuli used to prevent sleep. In this experiment, however, experimental and control rats received the same relatively mild physical stimuli, but stimulus presentations were timed to reduce sleep severely in experimental rats but not in controls. Experimental rats suffered severe pathology and death; control rats did not.

Adrenal Glands↗

Circadian temperature and wake rhythms of rats exposed to prolonged continuous illumination.

The purpose of this study was to simultaneously measure temperature and sleep in the rat under continuous illumination in an attempt to reveal properties of the underlying circadian oscillators. At first, the circadian rhythms of temperature and wake free-ran in parallel. Within weeks or months, circadian arrhythmicity developed in most animals. Both circadian rhythms eventually damped out, even at fairly low light intensities. The circadian rhythm of wake was weaker and disintegrated sooner than the circadian rhythm of temperature. Although the data did not rule out control by separate circadian oscillators, one for temperature and one for wake, a single oscillator model was sufficient to explain this phenomenon. Ultradian variations with a period of about 2-5 hr were superimposed upon the circadian rhythms. When the circadian rhythms damped out, the ultradian variations remained. The ultradian bursts of wake preceded the ultradian bursts of temperature, suggesting a causal relationship. On the other hand, the circadian rhythm of temperature could not be dependent on the circadian rhythm of wakefulness, because the temperature rhythm could persist while the wake rhythm was absent.

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Recovery sleep following sleep deprivation in intact and suprachiasmatic nuclei-lesioned rats.

Recovery sleep was studied for 3-5 days following 24 h of sleep deprivation (TSD) in normal rats and in rats lacking circadian rhythms (CRs) of sleep because of prior lesioning of the suprachiasmatic nuclei (SCN). One group of lesioned rats was run in constant dim light. Another lesioned group and an intact group were run on a 12:12 dark-light schedule with TSD and recovery beginning at lights-off. All groups showed immediate rebounds of high-amplitude NREM sleep and paradoxical sleep, confined mostly to the first 12-18 h of recovery, and decreases in moderate and low-amplitude NREM sleep during the first 6-12 h of recovery. Thus, sleep stage rebound priorities were little affected by CRs. Total sleep rebound was initially greatest in intact rats, but limited mostly to the first 12 h of recovery. Total sleep rebound was distributed over a longer period in SCN rats, but total accumulated rebound was similar in all groups. Thus, CRs appear to modulate the timing but not the amount of accumulated total sleep rebound. Results were interpreted in terms of ceiling effects on total sleep, delayed rebounds, and competition between CRs and homeostatic recovery processes. Recovery sleep of lesioned rats on the dark-light schedule was marked by a transient diurnal rhythm.

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Sleep in young and old rats.

Five young rats, age 152--175 days, and six old rats, age 782--801 days, all of the F-344 strain, were compared by electronic methods for amplitude of slow wave activity during sleep and for other sleep parameters. Unlike humans, who show a pronounced loss of slow wave activity with advanced age, no significant difference in delta activity could be detected between young and old rats. Several hypotheses about the species difference were reviewed. Young and old rats, however, did show several differences in other sleep parameters which parallel those observed in humans. These age-related changes were a moderate decrease in the percent of total sleep time spent in paradoxical sleep, a decrease in the length of sleep bouts, an increase in the number of sleep bouts, and a decrease in the amplitude of the diurnal rhythm of sleep.

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Ventral hippocampus spikes during sleep, wakefulness, and arousal in the cat.

The relationship between high amplitude (100--300- micro V) spike potentials (50--100 msec duration) in the ventral hippocampus (VH) and sleep-wakefulness stages was investigated. Forty-eight hours of continuous recordings taken from 5 chronically implanted cats were quantitatively scored for stage by digitized outputs of integrated EEG and electromyographic signals and for VH spikes by automatic devices. (1) A very strong relationship was observed between VH spike rates and EEG stage. Spikes were rare during wakefulness and paradoxical sleep (PS). They were always most frequent during nonrapid eye movement (NREM) sleep stages, progressively increasing through drowsiness, moderate amplitude slow wave activity, and high amplitude slow wave activity. (2) VH spike rates varied inversely with level of behavioral arousal within wakefulness. Rates were lowest during the presentation of novel experimental stimuli, higher during spontaneous movement, and highest during quiet wakefulness. (3) VH spikes anticipated stage changes independent of the quantified EEG. Spike rates increased from previous baseline levels in the 30 sec epoch of waking immediately preceding NREM sleep onset and in the transition period between PS and NREM sleep. They decreased significantly from previous base-line levels in the 30 sec epoch of NREM sleep preceding either waking or PS. These results show that the VH spike is a potentially useful noncortical indicator of NREM sleep. Within wakefulness and in the anticipation of stage changes it can be a more sensitive indicator of sleep processes or arousal level than the EEG.

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Effects of sleep deprivation on sleepiness, sleep intensity, and subsequent sleep in the rat.

The effects of 24 hr of sleep deprivation on cortical EEG and ventral hippocampus EEG recordings, ventral hippocampus spike rates, sleep stages percentages, and bout length measures were studied in rats. Two groups, differing only in the rate and distance they were forced to walk during deprivation by the water wheel method, were recorded continuously (23 hr per day) for one baseline, one deprivation, and two recovery days. During deprivation, microsleeps, increased hippocampal spike rates, and increased amplitude of the EEG recordings all suggested the intrusion of sleep processes. Nonetheless, there was no evidence to support the idea that these animals were not substantially deprived of sleep. No important differences were found in the recovery data of the two groups, even though one group walked three times as far as the other during deprivation. This supports the idea that, in conjunction with large amounts of sleep deprivation, changes in exercise and energy depletion may have little effect on sleep measures. During recovery, increased hippocampal spike rates and bout lengths, as well as increases in EEG amplitude, were interpreted in terms of increased sleep "intensity." High amplitude NREM sleep rebounded first, followed by rebounds in both paradoxical sleep and low amplitude NREM sleep. This pattern was compared to patterns previously reported for humans, cats, and rats. Finally, the tendency for some measures to fall below their baseline levels after an initial rebound was discussed in terms of "sleep inhibition" and servomechanism theory.

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Effect of thyroxine on sleep in the rat.

The relationships between daily sleep time and metabolic rate both in phylogeny and ontogeny have suggested that sleep functions in the regulation of an animal's energy expenditure. Smaller animals may sleep more to conserve more energy. The present study investigated whether, in individual animals, sleep increased in response to the administration of thyroxine, which increased metabolic rate. The sleep, motor activity, food intake, and weights of rats were sampled over a base-line period of 2--4 weeks, during 2--6 weeks of daily administration of thyroxine (150 or 300 microgram/kg), and during a recovery period of 2--4 weeks. In addition to comparisons among base-line, drug, and recovery periods, comparisons were also made with control animals recorded at the same time. Thyroxine produced the increases in food intake and decreases in weight gain which usually accompany increases in metabolic rate. In spite of this evidence of major systemic adjustments in energy input (increased food intake) and energy output (decreased growth) in response to the increased energy expenditure of a raised metabolic rate, there was no change in total sleep time. Therefore, the results do not support the theory that sleep adapts to prevailing energy demands. Although the rate of cycling through the sleep stages is also related to metabolic rate both in phylogeny and ontogeny, in this study thyroxine did not change the period of paradoxical sleep rhythm.

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