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At least 1,387 records · Page 77Linked to original sources
PubMed1989

Rapid eye movement sleep deprivation depresses plasma FSH and LH in castrated rats.

In castrated Wistar rats four days of Rapid Eye Movement sleep (REMs) deprivation by the cuff pedestal method induced decrements in plasma LH and FSH. The adenohypophyseal levels of these hormones were decreased in the REMs-deprived rats and in the control rats kept on pedestals with the supporting cuff in the elevated position as compared with the home-cage control rats. The results are discussed in terms of regional brain metabolic activity and transmission.

Animals↗
PubMed1982

Effects of paradoxical sleep deprivation on two-way avoidance acquisition.

Immediately following 72 hrs of paradoxical sleep (PS) deprivation, Wistar rats were given a shuttle-box avoidance task consisting of 50 trials. At an interval of 6 days retention was assessed through a reacquisition session of 20 trials. In a first experiment, the pendulum technique was employed for PS deprivation and its effects were compared with those produced by the conventional watertank technique. The first technique consists of arousing animals from sleep before PS can arise, by swinging their cages in a way that produces postural imbalance at regular intervals. A moving pendulum just not causing imbalance in the animals served as control for this technique. As control for the watertank technique the large platform was chosen. Shuttle-box avoidance was greatly impaired during the second half of the acquisition session in both platform conditions as compared to both pendulum conditions. A relatively small deficit was found toward the end of the session in both PS deprivation conditions as compared to both control conditions. No differences in avoidance were established during retention testing, suggesting that performance rather than learning deficits occurred during acquisition. In a second experiment, the multiple platform was used for PS deprivation. This modified version of the watertank technique also disrupted performance during shuttle-box avoidance acquisition. However, this effect appeared to be less pronounced than the effect found in the classical platform condition of Experiment 1. It is concluded that the performance deficit induced by both the classical and the multiple platform condition was mainly due to nonspecific effects.

Animals↗
PubMed2002

Rapid eye movement sleep deprivation modifies expression of long-term potentiation in visual cortex of immature rats.

During rapid eye movement (REM) sleep, activity of non-retinal origin is propagated into central visual-system pathways in a manner similar, in pattern and intensity, to central visual-system activity that is exogenously generated in waking. It has been hypothesized that REM sleep, which is more abundantly represented early in life than later, functions to provide adjunct 'afferent' input for shaping synaptic connectivity during brain maturation. Here we present data that support this proposal. Recent studies have described a developmentally regulated form of in vitro long-term potentiation (LTP) in the visual cortex that is experience- and age-dependent. In immature rats, suppression of retinal activation of the visual system by removal of visual experience (dark rearing) extends the age when the developmentally regulated form of LTP can be produced. This study tests whether suppression of REM-state activation of the visual system also lengthens the developmental period in which this specific form of LTP can be elicited. Young rats were deprived of REM sleep by the multiple-small-platforms-over-water method during the typically latest week for induction of such LTP in slices of visual cortex. After this week, we could still induce LTP in slices from nearly all the REM-sleep-deprived rats (8/9) but not from age-matched rats that had not lost REM sleep (0/5). The control rats had been housed on large platforms that allow the animals to obtain REM sleep. Only body weights and the concentration of thyrotrophin-releasing hormone in the hypothalamus distinguished home-caged, normal-sleeping controls from both groups of platform animals. On all measures, stress levels were not dissimilar in the two platforms groups. After 7 days of behavioral suppression of REM sleep in immature rats, and consequent reduction of the intense, extra-retinal activity endogenously generated during this sleep state, we found that the period was extended in which developmentally regulated synaptic plasticity (LTP) could be elicited in slices of visual neocortex. These studies support the role of REM sleep and its associated neuronal activity in brain maturation.

Aging↗
PubMed1993

REM sleep deprivation potentiates the effects of imipramine and desipramine but not that of clomipramine in the forced swimming test.

Effects of REM sleep (REMs) deprivation on the basal swimming activity and the tricyclic anti-depressants-induced increase in swimming activity in the forced swimming test were investigated. Immediately after a 48-hr period of REMs deprivation, the basal swimming activity in REMs-deprived mice was significantly higher than those in group-housed and socially isolated animals used as the control groups. The REMs deprivation-induced increase in the swimming activity was not changed by adrenoceptor antagonists and it returned to the control levels 3 hr after the REMs deprivation treatment. Moreover, imipramine and desipramine but not clomipramine further increased the swimming activity enhanced by REMs deprivation at doses that did not affect the activity in the control groups. The enhancing effect of REMs deprivation on the sensitivity to imipramine and desipramine remained unchanged even at 3 hr after the REMs deprivation treatment, and it was blocked by the alpha 2-adrenoceptor antagonist yohimbine. These results suggest that the REMs deprivation-induced increase in basal swimming activity in the forced swimming test is not mediated by adrenoceptor mechanisms, whereas the enhancing effect of REMs deprivation on the sensitivity to imipramine and desipramine may be mediated by the functional changes in alpha 2-adrenoceptors in the brain.

Adrenergic alpha-Antagonists↗
PubMed1990

Sleep deprivation headache.

Headaches due to insufficient or interrupted sleep are generally labelled "tension headaches" of psychogenic origin. In 25 healthy subjects, variable amounts of sleep loss (1-3 h for 1-3 nights) caused headaches lasting from 1 h to all day. The headache was most frequently a dull ache, a heaviness or a pressure sensation felt in the forehead and/or at the vertex. Simple analgesics, purchaseable without a doctor's prescription, completely or markedly reduced the head pain in 20-60 min. Headaches due to insufficient sleep differ from tension headaches in their site, duration and response to analgesics. Assuming that pain implies a regional dysfunction, headaches caused by sleep loss provide support for the notion that sleep has a restorative function in the brain.

Adult↗