Sleep deprivation expression

Maloney, K. J., Mainvilie, L. Jones, B. E. (1999). Differential c-Fos expression in cholinergic, monoaminergic, and GABAergic cell groups of the pontomesencephalic tegmentum after paradoxical sleep deprivation and recovery. J. Neurosci 19, 3057-72. 

Several studies suggest that cortistatin expression correlates with the sleep homeostat. The concentration of cortistatin mRNA oscillates with the light-dark cycle in rats, with maximal levels at the end of the dark (i.e. active) period. Further, the steady-state concentration of cortistatin mRNA increases four-fold after sleep deprivation, and returns to normal levels after sleep rebound, indicating that the expression of the peptide is associated with sleep demand (Spier de Lecea, 2000). Preliminary studies in cortical slices suggest that cortistatin-14 increases cortical synchronization by enhancing the H-current. Thus, cortistatin and somatostatin may be part of the intrinsic mechanisms of the cerebral cortex that are involved in the maintenance of excitability. 

Figure 4 PVT performance responses to varying doses of daily sleep. Mean PVT lapses per day (07 30-23 30), measured at 2-hr intervals, expressed relative to baseline (BL), in subjects randomized to an 8-hr (n = 9 open diamond), 6-hr (n = 13 open square), or 4-hr (n = 13 open circle) sleep opportunity per day for 14 consecutive days or 0-hr (n = 13 closed square) sleep condition across 3 days. The curves represent statistical nonlinear model-based best-fitting profiles of the PVT performance response to sleep loss. The mean ( s.e.m.) ranges of neurobehavioral functions for 1 and 2 days of total sleep deprivation (0 hr sleep) are illustrated by the light and dark bands, respectively, allowing comparison of the 3-day total sleep deprivation condition and the 14-day chronic sleep restriction conditions. (From Ref. 35.)...

In a laboratory-based study of sleepiness using the Multiple Sleep Latency Test (MSLT), hospital residents were found to be near the twilight zone following postcall (mean time to sleep of 5.5 min) (46). Perhaps most provocative was that their baseline (not on-call) level of sleepiness was not significantly different at 6.5 min. This demonstrated both the level of chronic sleep deprivation experienced (as reflected in the baseline condition) and the physiological level of sleepiness that can be expressed postcall. When the residents had the opportunity... 

V. Gene Expression During Sleep Deprivation and Recovery Sleep Candidate Gene Studies... 

Although the focus of the foregoing discussion has been on total SD and the subsequent RS, gene expression has also been studied in relation to selective SD. Selective REM sleep deprivation has been reported to increase the expression of... 

Cirelli C. How sleep deprivation affects gene expression in the brain a review of recent findings. J Appl Physiol 2002 92 394-400. 

O Hara BF, Young KA, Watson FL, Heller HC, Kilduff TS. Immediate early gene expression in brain during sleep deprivation preliminary observations. Sleep 1993 16 1-7. 

Terao A, Greco MA, Davis RW, Heller HC, Kilduff TS. Region-specific changes in immediate early gene expression in response to sleep deprivation and recovery sleep in the mouse brain. Neuroscience 2003 120 1115-1124. 

Neuner-Jehle M, Denizot JP, Borbely AA, Mallet J. Characterization and sleep deprivation-induced expression modulation of dendrin, a novel dendritic protein in rat brain neurons. J Neurosci Res 1996 46 138-151. 

Terao A, Steininger TL, Hyder K, et al. Differential increase in the expression of heat shock protein family members during sleep deprivation and during sleep. Neuroscience 2003 116 187-200. 

Toppila J, Stenberg D, Alanko L, et al. REM sleep deprivation induces galanin gene expression in the rat brain. Neurosci Lett 1995 183 171-174. 

Kushida CA, Zoltoski RK, Gillin JC. The expression of ml-m3 muscarinic receptor mRNAs in rat brain following REM sleep deprivation. Neuroreport 1995 6 1705-1708. 

Maloney KJ, Mainville L, Jones BE. c-Fos expression in dopaminergic and GABAergic neurons of the ventral mesencephalic tegmentum after paradoxical sleep deprivation and recovery. Eur J Neurosci 2002 15 774-778. 

Hypothalamic content and mRNA levels of TNF-a peak during the early light period, when NREM sleep is maximal, in the rat (70,71). IL-1-like activity varies with the sleep-wake cycle in the cerebrospinal fluid of cats (72). IL-lp protein levels in plasma (73) and hypothalamic IL-lp mRNA levels (74) are highest during the sleep period in rats. Sleep deprivation increases IL-ip and TNF-a mRNA levels in the hypothalamus (75-77) and expression of the 55-kD TNFR is also stimulated in the brain (77). In humans, peak levels of IL-1 occur at sleep onset in the blood (78) and IL-1 blood levels also increase during sleep deprivation (79). Blood levels of TNF-a correlate with EEG slow-wave activity (80), and concentrations of circulating TNF-a and the soluble 55-kD TNFR increase after sleep deprivation in humans (81). 

Mackiewicz M, Sollars PJ, Ogilvie MD, Pack AI. Modulation of IL-1 beta gene expression in the rat CNS during sleep deprivation. Neuroreport 1996 7 529-533. 

Taishi P, Gardi J, Chen Z, Fang J, Krueger JM. Sleep deprivation increases the expression of TNF alpha mRNA and TNF 55kD receptor mRNA in rat brain. Physiologist 1999 42 A4. 

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