Rapid eye movement sleep

About: Rapid eye movement sleep is a research topic. Over the lifetime, 3740 publications have been published within this topic receiving 183415 citations. The topic is also known as: REM sleep & REMS.

Intrapreoptic Microinjection of GHRH or Its Antagonist Alters Sleep in Rats

Abstract: Previous reports indicate that growth hormone-releasing hormone (GHRH) is involved in sleep regulation. The site of action mediating the nonrapid eye movement sleep (NREMS)-promoting effects of GHRH is not known, but it is independent from the pituitary. GHRH (0.001, 0. 01, and 0.1 nmol/kg) or a competitive antagonist of GHRH (0.003, 0.3, and 14 nmol/kg) was microinjected into the preoptic area, and the sleep-wake activity was recorded for 23 hr after injection in rats. GHRH elicited dose-dependent increases in the duration and in the intensity of NREMS compared with that in control records after intrapreoptic injection of physiological saline. The antagonist decreased the duration and intensity of NREMS and prolonged sleep latency. Consistent alterations in rapid eye movement sleep (REMS) and in brain temperature were not found. The GHRH antagonist also attenuated the enhancements in NREMS elicited by 3 hr of sleep deprivation. Histological verification of the injection sites showed that the majority of the effective injections were in the preoptic area and the diagonal band of Broca. The results indicate that the preoptic area mediates the sleep-promoting activity of GHRH.

Selective rapid eye movement sleep deprivation impairs the maintenance of long‐term potentiation in the rat hippocampus

Abstract: Rapid eye movement (REM) sleep deprivation (RSD) is known to impair learning and memory. Previous studies have demonstrated that RSD induces an impairment of hippocampal long-term potentiation (LTP). In most of these studies, RSD was set up prior to LTP induction. In this work, we focused on RSD after LTP induction. We investigated the effect of RSD for 24-48 h after induction of LTP in the dentate gyrus on LTP maintenance and whether a REM rebound after 48 h RSD affected LTP. RSD rats were deprived of REM sleep by stroking their backs using a brush, whereas control rats were allowed to sleep freely. Another control group of rats was awoken during non-REM sleep (NRS) under the same conditions (NRS group). REM-deprived rats displayed a faster decay of population spike amplitudes compared with the control and NRS groups over a 24-h recording time. After 48 h RSD, there was no difference in the population spike amplitudes before or after 4 h of release from RSD. These results suggest that REM sleep after LTP induction in the dentate gyrus plays an essential role in LTP maintenance, whereas a REM rebound does not restore the RSD-induced impairment of LTP.

Adjustment disorders of sleep: The sleep effects of a major stressful event and its resolution

Abstract: Seventy volunteers had 3 nights of sleep recordings during a period of marital separation, and 61 returned for repeat studies 1 year later. At that time, the divorce was final for 42. Forty of the volunteers were depressed when first screened, and 30 were not. Initially all those undergoing marital separation had less delta sleep than an age-matched married comparison sample. Delta increased at followup for those whose divorce was completed. Rapid eye movement (REM) latency was reduced and REM percent was elevated only in the depressed. Among the not depressed, those whose divorces remained incomplete at the followup had lower delta, higher REM percent, and shorter REM latency than did those whose divorces were finalized. This suggests that prolonged emotional stress may put these subjects at some risk for a mood disorder.

Increased activation of anterior paralimbic and executive cortex from waking to rapid eye movement sleep in depression.

Abstract: Background Depression is associated with sleep disturbances, including alterations in rapid eye movement (REM) sleep, that may relate to the neurobiology of the disorder. Given that REM sleep activates limbic and anterior paralimbic cortex and that depressed patients demonstrate increases in electroencephalographic sleep measures of REM, we hypothesized greater activation of these structures during waking to REM sleep in depressed patients. Design Subjects completed electroencephalographic sleep and regional cerebral glucose metabolism assessments during both waking and REM sleep using [ 18 F]fluoro-2-deoxy-D-glucose positron emission tomography. Setting Patients and healthy subjects recruited from the general community to participate in a research study of depression at an academic medical center. Patients Twenty-four unmedicated patients who met the Structured Clinical Interview for DSM-IV criteria for current major depression and who had a score of 15 or higher on a 17-item Hamilton Rating Scale for Depression; 14 medically healthy subjects of comparable age and sex who were free of mental disorders. Main Outcome Measures Electroencephalographic sleep, semiquantitative and relative regional cerebral metabolism during waking and REM sleep. Results Depressed patients showed greater REM sleep percentages. While both healthy and depressed patients activated anterior paralimbic structures from waking to REM sleep, the spatial extent of this activation was greater in the depressed patients. Additionally, depressed patients showed greater activation in bilateral dorsolateral prefrontal, left premotor, primary sensorimotor, and left parietal cortices, as well as in the midbrain reticular formation. Conclusions Increased anterior paralimbic activation from waking to REM sleep may be related to affective dysregulation in depressed patients. Increased activation of executive cortex may be related to a cognitive dysregulation. These results suggest that altered function of limbic/anterior paralimbic and prefrontal circuits in depression is accentuated during the REM sleep state. The characteristic sleep disturbances of depression may reflect this dysregulation.

Simultaneous Pontine and Basal Forebrain Microinjections of Carbachol Suppress REM Sleep

Abstract: This study was performed to test the hypothesis that cholinoceptive basal forebrain systems can significantly influence cholinoceptive pontine mechanisms known to be important for generating rapid eye movement (REM) sleep. This hypothesis was examined by microinjecting the cholinergic agonist carbachol or saline (vehicle control) into the pons, the basal forebrain, or simultaneously into the pons and basal forebrain, while quantifying the effects on sleep and wakefulness in unanesthetized, chronically instrumented cats. All microinjections were made during wakefulness and were followed by 2 or 4 hr of recording. Polygraphic records were scored for wakefulness, non-REM sleep, REM sleep, and the REM sleep-like state evoked by pontine administration of carbachol (DCarb). Dependent variables quantified following each microinjection included the percentage of recording time spent in each state, the latency to onset of non-REM, REM, and DCarb, the number of episodes per hour of each state, and the duration of the longest episode of each state. A total of 149 microinjections were made into 15 forebrain and 11 pontine sites in eight cats. Basal forebrain administration of carbachol significantly increased wakefulness. Pontine microinjection of carbachol produced a state that polygraphically and behaviorally resembled REM sleep. This REM sleep- like state occurred in amounts significantly greater than natural REM sleep. Pontine carbachol also significantly decreased wakefulness and non-REM sleep. Simultaneous injection of carbachol into the pons and basal forebrain enhanced REM sleep, but the magnitude of this enhancement was significantly less than the increase in REM sleep evoked by carbachol injection into the pons alone. The results show that cholinoceptive regions of the basal forebrain can increase wakefulness and reduce the ability of pontine carbachol to evoke the REM sleep-like state. These findings suggest that basal forebrain administration of carbachol activates an arousal-generating system that can successfully compete with the powerful cholinergic REM sleep- generating system of the pons.