Slow-wave sleep

About: Slow-wave sleep is a research topic. Over the lifetime, 6543 publications have been published within this topic receiving 320663 citations. The topic is also known as: deep sleep.

Effects of skilled training on sleep slow wave activity and cortical gene expression in the rat.

Abstract: Study objective: The best characterized marker of sleep homeostasis is the amount of slow wave activity (SWA, 05-4 Hz) during NREM sleep SWA increases as a function of previous waking time and declines during sleep, but the underlying mechanisms remain unclear We have suggested that SWA homeostasis is linked to synaptic potentiation associated with learning during wakefulness Indeed, studies in rodents and humans found that SWA increases after manipulations that presumably enhance synaptic strength, but the evidence remains indirect Here we trained rats in skilled reaching, a task known to elicit long-term potentiation in the trained motor cortex, and immediately after learning measured SWA and cortical protein levels of c-fos and Arc, 2 activity-dependent genes involved in motor learning Design: Intracortical local field potential recordings and training on reaching task Setting: Basic sleep research laboratory Patients or Participants: Long Evans adult male rats Interventions: N/A Measurements and Results: SWA increased post-training in the trained cortex (the frontal cortex contralateral to the limb used to learn the task), with smaller or no increase in other cortical areas This increase was reversible within 1 hour, specific to NREM sleep, and positively correlated with changes in performance during the prior training session, suggesting that it reflects plasticity and not just motor activity Fos and Arc levels were higher in the trained relative to untrained motor cortex immediately after training, but this asymmetry was no longer present after 1 hour of sleep Conclusion: Learning to reach specifically affects gene expression in the trained motor cortex and, in the same area, increases sleep need as measured by a local change in SWA

Hypersomnia in bipolar depression: a comparison with narcolepsy using the multiple sleep latency test.

Abstract: Objective: This study characterized objectively the hypersomnia frequently seen in the depressed phase ofbipolar affective disorder. On the basis ofprevious work in sleep and affective disorders, it has been hypothesized that the hypersomnia is related to greater REM sleep. This hypothesis was tested by using a multiple sleep latency test to compare bipolar affective disorder with narcolepsy, a well-defined primary sleep disorder associated with known REM sleep dysfunction. Method: Twenty-five bipolar depressed patients were selected on the basis ofcomplaints ofhypersomnia. They underwent 2 nights ofpolysomnography followed by a multiple sleep latency test. Data on their nocturnal sleep and daytime naps were compared with similar data on 23 nondepressed narcoleptic patients referred for sleep evaluation. & �yjj�� Despite their complaints of hypersomnia, no abnormalities were noted for the bipolar group in the results from the multiple sleep latency test. Contrary to the working hypothesis, REM sleep was notably absent during daytime naps in the depressed patients, in marked contrast to the findings for the narcoleptic group. Conclusions: The complaint of sleepiness in the hypersomnic bipolar depressed patient appears to be related to the lack of interest, withdrawal, decreased energy, or psychomotor retardation inherent in the anergic depressed condition, rather than an increase in true sleep propensity or REM sleep propensity. (AmJ Psychiatry1991; 148:1177-1181)

Generalized anxiety and sleep architecture: A polysomnographic investigation.

Abstract: The sleep of 15 adult subjects who reported heightened generalized anxiety in the absence of other psychiatric syndromes and a 15-adult contrast group were studied by means of nocturnal polysomnography. Analysis of polysomnography variables revealed a significant discriminant function that accounted for 79% of the variance between groups, indicating that high-anxiety/worry subjects took longer to fall asleep, had a smaller percentage of deep (slow-wave) sleep, and more frequent transitions into light sleep [stage 1 nonrapid eye movement (NREM)]. Additional analyses indicated that high-anxiety/worry subjects had a greater percentage of light sleep, more early microarousals, a lower rapid eye movement (REM) density relative to low-anxiety subjects. These subjects also showed more electrodermal storming when slow-wave sleep and REM sleep variables were covaried. Results indicated disrupted sleep depth and continuity similar to that documented in clinical anxiety disorder patients and distinct from that of depressed patients. These results indicate that generalized anxiety and worry in otherwise healthy individuals may act to produce a clinically significant sleep disturbance in the absence of other psychiatric symptoms.

Hypothalamo‐preoptic Histaminergic Projections in Sleep‐Wake Control in the Cat

Abstract: Cats were chronically implanted with electrodes for polygraphic recordings and cannulae for intracerebral microinjections in order to study the functional role of histaminergic innervation of the preoptic-anterior hypothalamus in sleep-wake control. alpha-Fluoromethylhistidine (alpha FMH, 50 micrograms in 1 microliter), a specific inhibitor of the histamine-synthesizing enzyme, when injected bilaterally into the preoptic area, where numerous histaminergic fibres and terminal-like structures are present, caused a significant increase in deep slow wave sleep (S2) and paradoxical sleep (PS) and a decrease in wakefulness. In contrast, microinjections of histamine (5 or 30 micrograms in 1 microliter) in the same area dose-relatedly increased wakefulness and decreased both slow wave sleep and paradoxical sleep. The effects of histamine were reduced by pretreatment with mepyramine (1 mg/kg i.p.), a well known histamine H1 receptor antagonist, and were mimicked by a local injection of impromidine (1 microgram in 1 microliter), a potent histamine H2 receptor agonist. Microinjections of mepyramine alone (120 micrograms in 1 microliter) caused an increase in slow wave sleep. These results suggest that preoptic histaminergic innervation is involved in sleep-wake control and that the action might be mediated via both H1 and H2 receptors.

REM SLEEP DEPRIVATION AND LONG-TERM POTENTIATION Paradoxical (REM) Sleep Deprivation Causes a Large and Rapidly Reversible Decrease in Long-Term Potentiation, Synaptic Transmission, Glutamate Receptor Protein Levels, and ERK/MAPK Activation in the Dorsal Hippocampus

Abstract: 5 These authors equally contributed to the present work Study Objectives: It has been shown that wake (W) and slow wave sleep (SWS) modulate synaptic transmission in neocortical projections. However the impact of paradoxical sleep (PS) quantities on synaptic transmission remains unknown. We examined whether PS modulated the excitatory transmission and expression of glutamate receptor sub- types and phosphorylated extracellular signal-regulated kinases (p- ERK1/2). Design: PS deprivation (PSD) was carried out with the multiple plat- forms method on adult male Sprague-Dawley rats. LTP, late-LTP, and synaptic transmission were studied in the dorsal and ventral hippocam- pus of controls, 75-h PSD and 150-min PS rebound (PSR). GluR1 and NR1 protein and mRNA expression were evaluated by western blot and real-time PCR. P-ERK1/2 level was quantified by western blot and im- munohistochemistry. Measurement and Results: PSD decreased synaptic transmission and LTP selectively in dorsal CA1 and PSR rescued these deficits. PSD-induced synaptic modifications in CA1 were associated with a decrease in GluR1, NR1, and p-ERK1/2 levels in dorsal CA1 without change in GluR1 and NR1 mRNA expression. Regression analysis shows that LTP is positively correlated with both PS quantities and SWS episodes duration, whereas synaptic transmission and late-LTP are positively correlated with PS quantities and negatively correlated with SWS quantities. Conclusions: These findings unveil previously unrecognized roles of PSD on synaptic transmission and LTP in the dorsal, but not in the ventral, hippocampus. The fact that the decrease in protein expression of GluR1 and NR1 was not associated with a change in mRNA expres- sion of these receptors suggests that a sleep-induced modulation of translational mechanisms occurs in dorsal CA1.