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Recovery Sleep (recovery + sleep)
Selected AbstractsCharacterization of sleep,wake patterns in a novel transgenic mouse line overexpressing human prepro-orexin/hypocretinACTA PHYSIOLOGICA, Issue 3 2010K. A. Mäkelä Abstract Aim:, Orexin/hypocretin peptides are expressed in the lateral hypothalamus and involved in the regulation of autonomic functions, energy homeostasis and arousal states. The sleep disorder narcolepsy, which is characterized by excessive daytime sleepiness and occurrence of sudden rapid eye movement (REM) sleep, is associated with a loss of orexin neurones. Our study investigated the effects of orexins on sleep,wake patterns in a novel transgenic mouse line overexpressing the human prepro-orexin (hPPO) gene under the control of its endogenous promoter. Methods:, Orexin overexpression was investigated by PCR, Southern and Western blotting as well as immunohistochemistry. Polysomnographic recordings were performed for analyses of sleep,wake patterns and for electroencephalographic activity during 24 h baseline and during and after 6 h of sleep deprivation (SD). Results:, Transgenic hPPO mice had increased expression of human prepro-orexin (hPPO) and orexin-A in the hypothalamus. Transgene expression decreased endogenous orexin-2 receptors but not orexin-1 receptors in the hypothalamus without affecting orexin receptor levels in the basal forebrain, cortex or hippocampus. Transgenic mice compared with their wild type littermates showed small but significant differences in the amount of waking and slow wave sleep, particularly during the light,dark transition periods, in addition to a slight reduction in REM sleep during baseline and during recovery sleep after SD. Conclusion:, The hPPO-overexpressing mice show a small reduction in REM sleep, in addition to differences in vigilance state amounts in the light/dark transition periods, but overall the sleep,wake patterns of hPPO-overexpressing mice do not significantly differ from their wild type littermates. [source] Functional topography of the human nonREM sleep electroencephalogramEUROPEAN JOURNAL OF NEUROSCIENCE, Issue 12 2001Luca A. Finelli Abstract The sleep EEG of healthy young men was recorded during baseline and recovery sleep after 40 h of waking. To analyse the EEG topography, power spectra were computed from 27 derivations. Mean power maps of the nonREM sleep EEG were calculated for 1-Hz bins between 1.0 and 24.75 Hz. Cluster analysis revealed a topographic segregation into distinct frequency bands which were similar for baseline and recovery sleep, and corresponded closely to the traditional frequency bands. Hallmarks of the power maps were the frontal predominance in the delta and alpha band, the occipital predominance in the theta band, and the sharply delineated vertex maximum in the sigma band. The effect of sleep deprivation on EEG topography was determined by calculating the recovery/baseline ratio of the power spectra. Prolonged waking induced an increase in power in the low-frequency range (1,10.75 Hz) which was largest over the frontal region, and a decrease in power in the sigma band (13,15.75 Hz) which was most pronounced over the vertex. The topographic pattern of the recovery/baseline power ratio was similar to the power ratio between the first and second half of the baseline night. These results indicate that changes in sleep propensity are reflected by specific regional differences in EEG power. The predominant increase of low-frequency power in frontal areas may be due to a high ,recovery need' of the frontal heteromodal association areas of the cortex. [source] Patterns of performance degradation and restoration during sleep restriction and subsequent recovery: a sleep dose-response studyJOURNAL OF SLEEP RESEARCH, Issue 1 2003Gregory Belenky SUMMARY Daytime performance changes were examined during chronic sleep restriction or augmentation and following subsequent recovery sleep. Sixty-six normal volunteers spent either 3 (n = 18), 5 (n= 16), 7 (n = 16), or 9 h (n = 16) daily time in bed (TIB) for 7 days (restriction/augmentation) followed by 3 days with 8 h daily TIB (recovery). In the 3-h group, speed (mean and fastest 10% of responses) on the psychomotor vigilance task (PVT) declined, and PVT lapses (reaction times greater than 500 ms) increased steadily across the 7 days of sleep restriction. In the 7- and 5-h groups speed initially declined, then appeared to stabilize at a reduced level; lapses were increased only in the 5-h group. In the 9-h group, speed and lapses remained at baseline levels. During recovery, PVT speed in the 7- and 5-h groups (and lapses in the 5-h group) remained at the stable, but reduced levels seen during the last days of the experimental phase, with no evidence of recovery. Speed and lapses in the 3-h group recovered rapidly following the first night of recovery sleep; however, recovery was incomplete with speed and lapses stabilizing at a level comparable with the 7- and 5-h groups. Performance in the 9-h group remained at baseline levels during the recovery phase. These results suggest that the brain adapts to chronic sleep restriction. In mild to moderate sleep restriction this adaptation is sufficient to stabilize performance, although at a reduced level. These adaptive changes are hypothesized to restrict brain operational capacity and to persist for several days after normal sleep duration is restored, delaying recovery. [source] Long-term vs. short-term processes regulating REM sleepJOURNAL OF SLEEP RESEARCH, Issue 1 2002PAUL FRANKEN In cats, rats, and mice, the amount of rapid eye movement sleep (REMS) lost during a sleep deprivation (SD) predicts the subsequent REMS rebound during recovery sleep. This suggests that REMS is homeostatically regulated and that a need or pressure for REMS accumulates in its absence, i.e. during both wakefulness and non-rapid eye movement sleep (NREMS). Conversely, it has been proposed that REMS pressure accumulates exclusively during NREMS [Benington and Heller, Am. J. Physiol. 266 (1994) R1992; Prog. Neurobiol. 44 (1994b) 433]. This hypothesis is based on the analysis of the duration of successive NREMS and REMS episodes and of electroencephalogram (EEG) events preceding REMS. Pre-REMS events (PREs) do not always result in sustained REMS and can thus be regarded as REMS attempts that increase as NREMS progresses. It is assumed that two processes regulating REMS can resolve the apparent contradiction between these two concepts: a `long-term' process that homeostatically regulates the daily REMS amount and a `short-term' process that regulates the NREM,REMS cycle. These issues were addressed in two SD experiments in rats. The two SDs varied in length (12 and 24 h) and resulted in very similar compensatory changes in NREMS but evoked very different changes for all REMS parameters studied. The large REMS increase observed after 24-h SD was accompanied by a reduction in unsuccessful PREs and an increase in sustained REMS episodes, together resulting in a threefold increase in the success-rate to enter REMS. Changes in success-rate matched those of a theoretically derived long-term REMS pressure. The SD induced changes in sleep architecture could be reproduced by assuming that the increased long-term REMS pressure interacts with the short-term process by increasing the probability to enter and remain in REMS. [source] | ||||||||||