Sleep analysis and a simple technique for selective deprivation of low-voltage, fast-wave sleep in a species of deermouse, P. m. bairdi (original) (raw)
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Sleep-deprivation: Effects on sleep and EEG in the rat
Journal of Comparative Physiology A-neuroethology Sensory Neural and Behavioral Physiology, 1979
The vigilance states (waking, rapid eye movement (REM) sleep, and non-REM (NREM) sleep), motor activity, food intake and water intake were continuously recorded by telemetry in unrestrained rats. In addition, an amplitude measure and a frequency measure (number of zero-crossings (ZCR) per 10 s) of the telemetered EEG-signal was obtained. The animals were recorded during a control day, then subjected to 12-h or 24-h sleep-deprivation (SD) by means of a slowly rotating cylinder, and subsequently recorded for further 1–2 days. The EEG-parameters were recorded also during SD. On the control day, the EEG-amplitude of NREM-sleep exhibited a decreasing trend in the 12-h light-phase (Figs. 3, 4). The occurence of slow wave sleep (SWS; defined as the NREM-sleep fraction with less than 40 ZCR/10 s) was practically limited to the first part of the light-phase (Figs. 2, 4). Cumulative plots of the zero-crossing bands (Fig. 2) revealed a prominent daily rhythm in the EEG-frequency distributionwithin NREM-sleep. The percentage of NREM-sleep and REM-sleep was little affected by the 12-h SD, but the amount of SWS and the EEG-amplitude of NREM-sleep were increased (Figs. 4, 6). After a 24-h SD period terminating before light-onset, NREM-sleep was reduced and REM-sleep was markedly enhanced (Figs. 4, 6; Table 1). Both the duration and frequency of REM-sleep episodes were increased, and episodes of total sleep prolonged (Table 2). The amount of SWS was significantly more increased after 24-h SD than after 12-h SD, whereas the EEG-amplitude of NREM-sleep was enhanced to a similar extent after both SD-schedules (Tables 1, 3 Fig. 6). After a 24-h SD period terminating before dark-onset, sleep (particularly REM-sleep) was enhanced in the first hours of the dark-phase, yet the usual high activity bouts prevailed in the later part of the dark-phase (Figs. 7, 8; Table 1). The extent and time-course of REM-sleep rebound was similar after the two 24-SD schedules, whereas SWS-rebound was different: SWS exhibited a one-stage rebound when recovery started in the light-phase, and a two-stage rebound when recovery started in the dark-phase (Fig. 9). A comparison of the effects of 12-h SD performed with the usual and with the double cylinder rotation rate, showed only small differences, indicating that forced locomotion was a minor factor in comparison to sleep-deprivation (Fig. 10; Table 1). The daily pattern of SWS on control days, and the marked increase of SWS after SD correspond to the results from other animal and human studies. It is proposed that due to the existence of an intensity dimension, NREM-sleep is finely regulated around its baseline level, and thus may be readily and accurately adjusted to current ‘needs’, whereas REM-sleep, lacking an apparent intensity gradient, is regulated around a level which is considerably below baseline. Thus, in contrast to NREM-sleep, REM-sleep compensation can occur only by an increase in the time devoted to this state, thereby curtailing the time available for other activities.
Natural Sleep Modifies the Rat Electroretinogram
Proceedings of The National Academy of Sciences, 1994
We show here electretinograms (ERGs) recorded from freely moving rats during sleep and wakefulness. Bilateral ERGs were evoked by flashes delivered through a light-emitting diode implanted under the skin above one eye and recorded through electrodes inside each orbit near the optic nerve. AdditI electrodes over each visual cortex monitored the brain waves and collected flash-evoked cortical potentials to compare with the ERGs. Connections to the stimulating and rdng ruments through a plug on the head made data collection posslble at any time without physically disturbing the annl. The three major n gs are (A) the ERG amplitude during slow-wave sleep can be 2 or more times that of the waking response; (iu) the ERG patter in slow-wave and REM sleep aite different; and (Mi) the sleep-
Sleep, 1992
Electroencephalograms (EEGs) of the cortex and of seven subcortical structures were recorded during two baseline days and during a recovery day following a l2-hour period of sleep deprivation (SD) in eight cats. The EEGs were analyzed by visual scoring and by spectral analysis. The following subcortical structures were studied: hippocampus, amygdala, hypothalamus, nucleus centralis lateralis of the thalamus, septum, nucleus caudatus and substantia nigra. The EEGs of all brain structures exhibited sleep state-dependent changes. In general, slow-wave activity (SWA, 0.5-4.0 Hz) during nonrapideye movement (NREM) sleep exceeded that of REM sleep. The power spectra (0.5-24.5 Hz) in NREM, as well as the relationship between the power spectra ofNREM and REM sleep, differed between the recording sites. Moreover, the rate of increase ofSWA in the course of an NREM episode and the rate of decrease of SW A at the transition from NREM to REM sleep differed between the brain structures. During the first 12 hours following SD, the duration of NREM increased due to a prolongation of the NREM episodes. REM increased by a rise in the number of REM episodes. During the same period, the NREM EEG power density in the delta and theta frequencies was enhanced in all brain structures. Furthermore, in all structures the enhancement of SW A was most pronounced at the beginning of the recovery period and gradually declined thereafter. SD also induced a rise in the rate of increase of SWAin the NREM episodes in all recording sites. This indicates that the enhancement of EEG power density was not only due to prolongation of the NREM episodes. The EEG activity during REM was barely affected by the SD. It is concluded that, in all brain structures studied, the EEG during NREM is characterized by high levels ofSW A. Furthermore, in each brain structure, SWA within NREM sleep is enhanced after a prolonged vigil. These data may indicate that SW A reflects a recovery process in cortical and subcortical structures.
The ontogeny of mammalian sleep: a response to Frank and Heller (2003)
Journal of Sleep Research, 2005
SUMMAR Y In a recent review, provided support for their Ôpresleep theoryÕ of sleep development. According to this theory, rapid eye movement (REM) and non-rapid eye movement (Non-REM) sleep in rats emerge from a common ÔdissociatedÕ state only when the neocortical EEG differentiates at 12 days of age (P12). Among the assumptions and inferences associated with this theory is that sleep before EEG differentiation is only Ôsleep-likeÕ and can only be characterized using behavioral measures; that the neural mechanisms governing presleep are distinct from those governing REM and Non-REM sleep; and that the presleep theory is the only theory that can account for developmental periods when REM and Non-REM sleep components appear to overlap. Evidence from our laboratory and others, however, refutes or casts doubt on these and other assertions. For example, infant sleep in rats is not Ôsleep-likeÕ in that it satisfies nearly every criterion used to characterize sleep across species. In addition, beginning as early as P2 in rats, myoclonic twitching occurs only against a background of muscle atonia, indicating that infant sleep is not dissociated and that electrographic measures are available for sleep characterization. Finally, improved techniques are leading to new insights concerning the neural substrates of sleep during early infancy. Thus, while many important developmental questions remain, the presleep theory, at least in its present form, does not accurately reflect the phenomenology of infant sleep.
Effect of sleep deprivation on sleep and EEG power spectra in the rat
Behavioural Brain Research, 1984
EEG power spectra of the rat were computed for consecutive 4-s epochs of the daily light period and matched with the scores of the vigilance states. Sleep was characterized by a progressive decline of low frequency spectral values (i.e. slow wave activity) in non-rapid eye movement (non-REM) sleep, and a progressive increase in the amount of REM sleep. During recovery from 24-h total sleep deprivation (TSD) the following changes were observed: an increase of slow wave activity in non REM sleep with a persisting declining trend; an enhancement of theta activity (7.25-10.0 Hz) both in REM sleep and waking; a decrease of non-REM sleep and an increase of REM sleep. In addition, a slow wave EEG pattern prevailed in the awake and behaving animal during the initial recovery period. In selective sleep deprivation paradigms, either REM sleep or slow wave activity in non-REM sleep was prevented during a 2-h period following upon 24-h TSD. During both procedures, non-REM sleep spectra in the lowest frequency band showed no increase. There was no evidence for a further enhancement of slow wave activity after its selective deprivation. The results indicate that: (1) slow wave activity in non-REM sleep and theta activity in REM sleep may reflect sleep intensity; and (2) REM sleep and active waking, the two states with dominant theta activity, may be functionally related.
Journal of Sleep Research, 2009
Studies on homeostatic aspects of sleep regulation have been focussed upon non-rapid eye movement (NREM) sleep, and direct comparisons with regional changes in rapid eye movement (REM) sleep are sparse. To this end, evaluation of electroencephalogram (EEG) changes in recovery sleep after extended waking is the classical approach for increasing homeostatic need. Here, we studied a large sample of 40 healthy subjects, considering a full-scalp EEG topography during baseline (BSL) and recovery sleep following 40 h of wakefulness (REC). In NREM sleep, the statistical maps of REC versus BSL differences revealed significant fronto-central increases of power from 0.5 to 11 Hz and decreases from 13 to 15 Hz. In REM sleep, REC versus BSL differences pointed to significant fronto-central increases in the 0.5-7 Hz and decreases in the 8-11 Hz bands. Moreover, the 12-15 Hz band showed a fronto-parietal increase and that at 22-24 Hz exhibited a fronto-central decrease. Hence, the 1-7 Hz range showed significant increases in both NREM sleep and REM sleep, with similar topography. The parallel change of NREM sleep and REM sleep EEG power is related, as confirmed by a correlational analysis, indicating that the increase in frequency of 2-7 Hz possibly subtends a state-aspecific homeostatic response. On the contrary, sleep deprivation has opposite effects on alpha and sigma activity in both states. In particular, this analysis points to the presence of state-specific homeostatic mechanisms for NREM sleep, limited to <2 Hz frequencies. In conclusion, REM sleep and NREM sleep seem to share some homeostatic mechanisms in response to sleep deprivation, as indicated mainly by the similar direction and topography of changes in low-frequency activity.