Biomedical subjects

A Rechtschaffen

Publications and source records attributed to A Rechtschaffen.

At least 37 records · Page 2Linked to original sources

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↗

PubMed1992

Sleep deprivation in the rat: XVI. Effects in a light-dark cycle.

To avoid a possible confound between the effects of sleep loss and disturbed circadian rhythms in previous studies of total sleep deprivation (TSD) by the disk-over-water method, TSD rats and their yoked control (TSC) rats had been maintained in constant light both before and during the experiment. With circadian rhythms of both groups flattened by constant light, group differences in outcome measures could be attributed to sleep loss. However, the constant light control entailed the possibility that the sleep loss effects might obtain only in constant light. To evaluate this possibility, three TSD-TSC rat pairs maintained on a 12 hour light: 12 hour dark (LD) schedule were studied. TSC rats showed only minor changes during the deprivation period. As in previous studies, TSD rats showed increased food intake; decreased weight; increased energy expenditure; debilitated appearance; lesions on the tail and paws; an initial increase followed by a large decrease in body temperature; impending death; and recovery sleep, which featured large, selective, sustained rebounds of paradoxical sleep and a reversal of all observed TSD-induced changes. Thus, TSD produced the same changes during an LD schedule as during constant light. The amplitude of the diurnal body temperature rhythm declined over the course of TSD and then almost completely recovered during the first day of recovery sleep. The decline was interpreted as the result of deprivation-induced thermoregulatory changes.

Animals↗

PubMed1991

Rat strain differences in response to dark pulse triggering of paradoxical sleep.

Previous studies of inbred rats have shown that Brown Norway (BN) rats had more daily paradoxical sleep (PS) than Lewis (L) rats, while F1 progeny had intermediate amounts, suggesting codominant or polygenic transmission. Amount of PS and the induction of PS episodes may be under separate genetic control. Earlier work had shown that five-minute exposures to cage lights-off every half-hour can trigger PS in outbred albino strains. To explore the genetic controls for PS induction, PS triggering by dark pulse stimulation was examined in L and BN rats. L rats showed a five-fold increase in PS during dark pulse stimulation. Although, as in the earlier study, BN rats had more total daily PS than L rats, they exhibited no dark pulse triggering of PS. Thus L and BN rats show significant strain differences in two independent parameters of PS, and may be a useful model for studying genetic and neurologic factors which regulate PS.

Animals↗

PubMed1991

Sleep deprivation in the rat: XII. Effect on ambient temperature choice.

Previous studies of total sleep deprivation in the rat by the disk-over-water method had shown an initial rise in body temperature (Tb), a later decline to below baseline levels, and a progressive rise in energy expenditure (EE). To evaluate the role of changes in temperature setpoint in these results, the ambient temperature choices (Tc) of six totally sleep-deprived (TSD) rats and their yoked control (TSC) rats were determined by the position in a thermally graded alley at which they chose to fall asleep. (Rats were removed from the alley and returned to the deprivation apparatus 1 min after sleep onset). Sleep deprivation was continued until TSD rats were near death. Tb and EE results were like those of the earlier studies. Tc rose progressively from 26.8 degrees C during baseline to 49.9 degrees C near the end of the deprivation period in TSD rats, whereas TSC rats showed only modest, nonsignificant increases. The attempt by TSD rats to get warmer, in spite of an elevated Tb, indicates a raised setpoint for behavioral thermoregulation and suggests that the increase in EE was also, at least in part, an attempt to reach an elevated setpoint. The progressively raised Tc also indicates that the late decline in Tb was a decline below setpoint rather than a response to a lower setpoint. Because EE increased, Tb decline must have resulted from excessive heat loss. Thus, TSD in the rat produced two thermoregulatory deficits-increased setpoint and excessive heat loss.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗

PubMed1991

Sleep deprivation in the rat: XIII. The effect of hypothyroidism on sleep deprivation symptoms.

Previous studies of rats subjected to total sleep deprivation by the disk-over-water method had shown a large increase in energy expenditure (EE) and an initial increase followed by a later decrease in body temperature (Tb). It had been proposed that the increase in Tb resulted from regulation toward a higher temperature or setpoint, that the later decline in Tb resulted from excessive heat loss, and that the increase in EE supported both of these thermoregulatory changes. To evaluate this proposed role of the increase in EE, we examined whether blunting the EE rise in sleep-deprived rats by making them hypothyroid attenuated and/or shortened the initial increase in Tb and accelerated the later decline in Tb. Rats made hypothyroid by propylthiouracil administration (TxD rats) were totally sleep deprived and compared to hypothyroid yoked control (TxC) rats and to previously studied, untreated, totally sleep-deprived (TSD) rats. Neither TxD nor TxC rats showed large increases in EE like those of TSD rats. TxD rats did not initially increase Tb, as TSD rats had. Presumably, TSD rats had been able to support an initially elevated Tb, in spite of excessive heat loss, by large increases in EE, although even these increases were eventually insufficient. TxD rats showed much earlier and greater declines in Tb than TxC and TSD rats, eventually becoming severely hypothermic. These results support the interpretation that the large increase in EE previously seen in TSD rats had been compensatory for deprivation-induced thermoregulatory deficits. TxD rats survived an average of 17.1 days, which was not significantly different from survival time in TSD rats. However, there were differences in mortal processes between the two groups. TxD rats died or were sacrificed after chronic, severe hypothermia without observable signs of other morbid pathology. TSD rats had not shown similarly low Tb until just prior to death, but had shown signs of severe pathology, including severely debilitated appearance, disheveled fur, and severe lesions on their tails and on the plantar surfaces of their paws. These signs were diminished or absent in TxD rats, possibly due to blunted EE, lower Tb, or other effects of hypothyroidism. Because the skin changes seen in TSD rats were minimal in TxD rats, they could not have been responsible for the excessive heat loss.

Adipose Tissue, Brown↗

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↗

PubMed1991

Cortical asymmetry of REM sleep EEG following unilateral pontine hemorrhage.

A 24-year-old woman with a left pontine hematoma showed marked asymmetry in the EEG of REM sleep, suggesting that a unilateral pontine lesion is sufficient to disrupt normal REM sleep EEG in the ipsilateral hemisphere. Other REM sleep characteristics (rapid eye movements, muscle atonia) were unaffected by this lesion.

Adult↗

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↗

PubMed1990

Effect of total sleep deprivation on 5'-deiodinase activity of rat brown adipose tissue.

Prolonged sleep deprivation of the rat produces a progressive increase in energy expenditure and an eventual decrease in body temperature, which suggests a profound derangement in thermoregulation. Because increased thermogenic activity in brown adipose tissue (BAT) is a likely mechanism mediating the observed increase in energy expenditure, we focused our attention on the effect of total sleep deprivation on BAT type II 5'-deiodinase (5'D-II), since its activation indicates BAT stimulation and is essential for full BAT thermogenic response. Five euthyroid rats were subjected to total (92%) sleep deprivation (euD-rats). Sharing the sleep deprivation apparatus, yoked control rats (euC-rats) received the same degree of physical stimulation as the D-rats, but were only partially (25%) sleep deprived. Additional cage controls (euCC-rats) were housed in the same room. Since during sleep deprivation the animals undergo a reduction in plasma T4 concentration and inability to maintain body temperature heralds death, an identical study was performed in five trios of hyperthyroid rats (hyperD-, hyperC-, and hyper CC-rats) given daily ip injections of 15 micrograms T4/100 g BW, 10 days before and throughout the deprivation period. Experiments were carried out at an ambient temperature of 29 C, close to thermoneutrality for rats. Sleep deprivation in hyperD-rats was maintained until death seemed imminent (9-14 days), and in euD-rats for 12-15 days. Sleep deprivation induced a significant increase in BAT 5'D-II activity in both hyperD- and euD-rats compared with that in euCC-rats (P less than 0.01). BAT 5'D-II in euC-rats was also significantly higher than that in euCC-rats (P less than 0.05), probably because they were partially sleep deprived. BAT 5'D-II activity in hyperD-rats was increased compared to that in both hyperC- and hyperCC-rats (P less than 0.05), in which the activity was slightly but not significantly lower than that in euCC-rats. No significant differences were observed in liver and kidney type I 5'-D (5'D-I) and in pituitary 5'D-II among euD-rats, euC-rats, and euCC-rats. As expected, the hyperthyroid groups (hyperD-rats, hyperC-rats, and hyperCC-rats) had significantly higher kidney 5'D-I and lower pituitary 5'D-II than the euCC-rats. Liver 5'D-I was also significantly increased in the hyperC-rats and hyperCC-rats, but not in the hyperD-rats. These observations indicate that total sleep deprivation is associated with a marked increase in BAT 5'D-II activity in both euthyroid and hyperthyroid rats.(ABSTRACT TRUNCATED AT 400 WORDS)

Acclimatization↗

PubMed1989

Sleep deprivation in the rat: I. Conceptual issues.

Sleep deprivation is a potentially powerful strategy for discovering the function(s) of sleep, but the approach has had limited success. Few studies have described serious physiological consequences of sleep deprivation, perhaps because the deprivation has not been maintained long enough. However, prolonging deprivation usually requires sustained, frequently intense stimulation, which makes it difficult to determine whether subsequent impairment resulted from the sleep loss or from the stimulation per se. Accordingly, several older studies that showed severe impairment have been neglected or discounted, because the impairment could have resulted from the stimulation. To evaluate the effects of sleep deprivation independent of the stimulation used to enforce deprivation, we have used an apparatus that can awaken experimental rats while delivering the same gentle stimulation to control rats according to a schedule that only moderately shortens their sleep.

Animals↗

PubMed1989

Sleep deprivation in the rat: III. Total sleep deprivation.

Ten rats were subjected to total sleep deprivation (TSD) by the disk apparatus. All TSD rats died or were sacrificed when death seemed imminent within 11-32 days. No anatomical cause of death was identified. All TSD rats showed a debilitated appearance, lesions on their tails and paws, and weight loss in spite of increased food intake. Their yoked control (TSC) rats remained healthy. Since dehydration was ruled out and several measures indicated accelerated use rather than failure to absorb nutrients, the food-weight changes in TSD rats were attributed to increased energy expenditure (EE). The measurement of EE, based upon caloric value of food, weight, and wastes, indicated that all TSD rats increased EE, with mean levels reaching more than twice baseline values.

Adrenal Glands↗

PubMed1989

Sleep deprivation in the rat: IV. Paradoxical sleep deprivation.

Twelve rats were subjected to paradoxical sleep deprivation (PSD) by the disk apparatus. All PSD rats died or were sacrificed when death seemed imminent within 16-54 days. No anatomical cause of death was identified. All PSD rats showed a debilitated appearance, lesions on their tails and paws, and weight loss in spite of increased food intake. Their yoked control (PSC) rats remained healthy. Since dehydration was ruled out and several measures indicated normal or accelerated use of nutrients, the food-weight changes in PSD rats were attributed to increased energy expenditure (EE). The measurement of EE, based upon caloric value of food, weight, and wastes, indicated that all PSD rats increased EE, with mean levels reaching more than twice baseline values. All of these changes had been observed in rats deprived totally of sleep; the major difference was that they developed more slowly in PSD rats.

Animals↗

PubMed1989

Sleep deprivation in the rat: V. Energy use and mediation.

We investigated the use and possible mechanisms mediating the increased energy expenditure (EE) previously described for rats subjected to total or paradoxical sleep deprivation. Bomb calorimetry of wastes showed that during deprivation the efficiency of energy utilization was not reduced. Estimates of CO2 production by the doubly labelled water method of indirect calorimetry correlated with EE estimated from the caloric value of food, weight change, and wastes and confirmed an increase in EE during deprivation. Core temperatures decreased during the later stages of deprivation, suggesting the hypothesis that excessive heat loss may have required increased EE to protect body temperature. The increased EE could not be explained by the metabolic cost of increase wakefulness, water exposure, or motor activity; an increase in resting EE was indicated. The contribution of the hypothalamic-pituitary-adrenal axis, thyroid gland, and sympathoadrenal system to the mediation of the EE increases was evaluated by measuring the plasma levels of their hormones. Results appear to rule out the first as a mediator. Evidence for the other two was equivocal.

Adrenal Cortex Hormones↗

PubMed1989

Sleep deprivation in the rat: VI. Skin changes.

All rats subjected to total or paradoxical sleep deprivation by the disk apparatus developed severe ulcerative and hyperkeratotic skin lesions localized to the plantar surfaces of their paws and to their tails. Yoked control rats only occasionally developed similar appearing lesions, which were always much less severe than in deprived rats. The deprived rat lesions could not be explained by pressure, disk rotation, water immersion, infection, necrotizing vasculitis, tyrosinemia, protein deficiency, or reduced rates of mitosis. Thus, although paw and tail lesions constitute a very reliable and severe symptom of total or selective sleep deprivation in the rat that potentially could yield insights into the pathogenic mechanisms induced by sleep loss, the mediation of the lesions remains unknown.

Animals↗

PubMed1989

Sleep deprivation in the rat: VII. Immune function.

Immune function studies were performed on splenic lymphocytes obtained from rats subjected to total or paradoxical sleep deprivation. Spleen cell counts, in vitro lymphocyte proliferation responses to mitogens, and in vitro and in vivo plaque-forming cell responses to antigens were obtained. Sleep-deprived rats were roughly equivalent to both their yoked controls and home-cage controls in all assays. The results do not support the hypothesis that sleep deprivation results in immune suppression as measured by the above-mentioned parameters.

Animals↗

PubMed1989

Sleep deprivation in the rat: II. Methodology.

Methods common to several studies in this series are described. A key feature is a sleep deprivation apparatus in which an experimental and a yoked control rat are housed on opposite sides of a divided disk suspended over shallow water. When the experimental rat enters a "forbidden" sleep stage, the disk is automatically rotated, forcing the experimental rat to walk to avoid being carried into the water. The control rat receives the same physical stimulation but can sleep ad lib when the disk is stationary.

Animals↗

PubMed1989

Sleep deprivation in the rat: VIII. High EEG amplitude sleep deprivation.

The disk apparatus was used to deprive six rats of the portion of non-rapid eye movement (NREM) sleep with high electroencephalogram (EEG) amplitude (HS2). All HS2 deprived (HS2D) rats died or were sacrificed when death seemed imminent within 23 to 66 days. No anatomical cause of death was identified. All deprived rats showed a debilitated appearance, lesions on their tails and paws, and weight loss in spite of increased food intake. Energy expenditure (calculated from the caloric value of food, weight change, and wastes) increased to more than twice baseline values. With one exception, yoked control rats remained generally healthy. It was not clear whether the changes in HS2D rats resulted from the loss of HS2 or the general disruption of NREM sleep that accompanied this loss. Also, it was not possible to produce major HS2 loss without incurring some loss of paradoxical sleep (PS). Control studies indicated that the partial PS loss in HS2D rats could not, in and of itself, account for all the pathological effects. However, an interaction of HS2D and partial PS loss in producing pathological effects cannot be ruled out.

Animals↗

PubMed1989

Sleep deprivation in the rat: IX. Recovery.

Eight rats were subjected to total sleep deprivation, paradoxical sleep deprivation, or high amplitude sleep deprivation until they showed major deprivation-induced changes. Then they were allowed to sleep ad lib. Three rats that had shown the largest temperature declines died within two to six recovery days. During the first 15 days of ad lib sleep, surviving rats showed complete or almost complete reversal of the following deprivation-induced changes: debilitated appearance, lesions on the paws and tail, high energy expenditure, large decreases in peritoneal temperature, high plasma epinephrine and norepinephrine levels, and low thyroxine levels. The most prominent features of recovery sleep in all rats were immediate and large rebounds of paradoxical sleep to far above baseline levels, followed by lesser temporally extended rebounds. Rebounds of high amplitude non-rapid eye movement (NREM) sleep occurred only in some rats and were smaller and less immediate.

Adrenal Cortex Hormones↗