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Recovery from Sleep Deprivation

Figure 12.1 Extracellular adenosine concentrations in different brain areas, measured with in vivo microdialysis from cats during sleep deprivation (6 h gentle handling) and recovery sleep. Concentrations are given as a percentage of pre-deprivation values. BF, basal forebrain CX, cingulate cortex TH, VA/VL nucleus of thalamus POA, preoptic hypothalamic area DRN, dorsal raphe nucleus PPT, pedunculopontine nucleus. In BF and CX adenosine rises during sleep deprivation, but starts to decline during deprivation in CX, whereas the decline occurs during recovery in the BF. In other areas there is no accumulation during sleep deprivation. Modified from Porkka-Heiskanen et al. (2000). Figure 12.1 Extracellular adenosine concentrations in different brain areas, measured with in vivo microdialysis from cats during sleep deprivation (6 h gentle handling) and recovery sleep. Concentrations are given as a percentage of pre-deprivation values. BF, basal forebrain CX, cingulate cortex TH, VA/VL nucleus of thalamus POA, preoptic hypothalamic area DRN, dorsal raphe nucleus PPT, pedunculopontine nucleus. In BF and CX adenosine rises during sleep deprivation, but starts to decline during deprivation in CX, whereas the decline occurs during recovery in the BF. In other areas there is no accumulation during sleep deprivation. Modified from Porkka-Heiskanen et al. (2000).
As early as in 1909, it was recognized that some chemical factor in the brain was responsible for recovery sleep. Cerebrospinal fluid (Legendre Pieron, 1911) or brain extract (Ishimori, 1909) from sleep-deprived dogs resulted in excess sleep when infused into the cerebral ventricles of recipient animals. The fact that the material was ineffective if heated or ultrafiltered pointed to a protein or peptide as sleep factor (Legendre Pieron, 1911). Later studies have... [Pg.337]

Until recently, it has been assumed that the performance effects of chronic sleep restriction were a milder version of the effects of acute, total sleep deprivation and that recovery from both was rapid once normal amounts of sleep were restored. Results from a study recently completed in our laboratory suggest that this may not be the case. [Pg.292]

The pattern of adaptation to chronic sleep restriction punctuated with acute, total sleep deprivation and rapid recovery from the latter may yield the types of changes in performance depicted in Fig. 2. Across the three armed services, in combat operations and in training for combat operations, severe total sleep deprivation is rare. Much more common for all is chronic, moderate sleep restriction at levels that would be expected to produce stable, albeit degraded performance. [Pg.293]

Zenko CE, Bergmann BM, Rechtschaffen A. Vascular resistance in the rat during baseline, chronic total sleep deprivation, and recovery from total sleep deprivation. Sleep 2000 23 341-346. [Pg.500]


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