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Roxanne Sterniczuk,1–3 Benjamin Rusak,1,2 Kenneth Rockwood31Department of Psychology and Neuroscience, Dalhousie University, Halifax, NS, 2Department of Psychiatry, Dalhousie University, Queen Elizabeth II Health Sciences Centre, Halifax, NS, 3Division of Geriatric Medicine, Department of Medicine, Queen Elizabeth II Health Sciences Centre, Halifax, NS, CanadaAbstract: Maintaining a stable and adequate sleeping pattern is associated with good health and disease prevention. As a restorative process, sleep is important for supporting immune function and aiding the body in healing and recovery. Aging is associated with characteristic changes to sleep quantity and quality, which make it more difficult to adjust sleep–wake rhythms to changing environmental conditions. Sleep disturbance and abnormal sleep–wake cycles are commonly reported in seriously ill older patients in the intensive care unit (ICU). A combination of intrinsic and extrinsic factors appears to contribute to these disruptions. Little is known regarding the effect that sleep disturbance has on health status in the oldest of old (80+), a group, who with diminishing physiological reserve and increasing prevalence of frailty, is at a greater risk of adverse health outcomes, such as cognitive decline and mortality. Here we review how sleep is altered in the ICU, with particular attention to older patients, especially those aged ≥80 years. Further work is required to understand what impact sleep disturbance has on frailty levels and poor outcomes in older critically ill patients.Keywords: intensive care unit, sleep–wake rhythm, aging, frailty

To understand how female sex hormones influence homeostatic mechanisms of sleep, we studied the effects of estradiol ([E.sub.2]) replacement on c-Fos immunoreactivity in sleep/ wake-regulatory brain areas after sleep deprivation (SD) in ovariectomized rats. Adult rats were ovariectomized and implanted subcutaneously with capsules containing 17[beta]-[E.sub.2] (10.5 [micro]g; to mimic diestrous [E.sub.2] levels) or oil. After 2 wk, animals with [E.sub.2] capsules received a single subcutaneous injection of 17[beta]-[E.sub.2] (10 [micro]g/kg; to achieve proestrous [E.sub.2] levels) or oil; control animals with oil capsules received an oil injection. Twenty-four hours later, animals were either left undisturbed or sleep deprived by 'gentle handling' for 6 h during the early light phase, and killed. [E.sub.2] treatment increased serum [E.sub.2] levels and uterus weights dose dependently, while attenuating body weight gain. Regardless of hormonal conditions, SD increased c-Fos immunoreactivity in all four arousal-promoting areas and four limbic and neuroendocrine nuclei studied, whereas it decreased c-Fos labeling in the sleep-promoting ventrolateral preoptic nucleus (VLPO). Low and high [E.sub.2] treatments enhanced the SD-induced c-Fos immunoreactivity in the laterodorsal subnucleus of the bed nucleus of stria terminalis and the tuberomammillary nucleus, and in orexin-containing hypothalamic neurons, with no effect on the basal forebrain and locus coeruleus. The high [E.sub.2] treatment decreased c-Fos labeling in the VLPO under nondeprived conditions. These results indicate that [E.sub.2] replacement modulates SD-induced or spontaneous c-Fos expression in sleep/wake-regulatory and limbic forebrain nuclei. These modulatory effects of [E.sub.2] replacement on neuronal activity may be, in part, responsible for [E.sub.2]'s influence on sleep/wake behavior. ovariectomy; immunohistochemistry: orexin/hypocretin; tuberomammillary nucleus; ventrolateral preoptic nucleus

BACKGROUND: Partial or total overnight sleep deprivation produces immediate mood improvement in about 50% of patients with depression, but not in healthy controls. Our objectives were to compare the neurochemical changes that accompanied partial overnight sleep deprivation in healthy and depressed participants, and to compare baseline neurochemical profiles and overnight neurochemical changes between those depressed participants who did and did not respond to sleep loss with mood improvement. METHODS: We studied 2 brain regions (left dorsal prefrontal area and pons) in 12 women with unipolar depression and in 15 healthy women using proton magnetic resonance spectroscopy acquired at 1.5 T. The scans took place at baseline and 24 hours later after a night with sleep restricted to a maximum of 2.5 hours (22:30-01:00). We assessed 3 neurochemical signals (referenced to internal water): N-acetylaspartate (NAA), choline compounds (Cho) and creatine-plus-phosphocreatine (tCr). RESULTS: In both groups combined, sleep restriction caused a 20.1% decrease in pontine tCr (F(1-16) = 5.07, p = 0.039, Cohen's d = 0.54) and an 11.3% increase in prefrontal Cho (F(1-21) = 5.24, p = 0.033, Cohen's d = 0.46). Follow-up tests revealed that prefrontal Cho increases were significant only among depressed participants (17.9% increase, t(9) = -3.35, p = 0.008, Cohen's d = 1.06). Five depressed patients showed at least 30% improvement in mood, whereas 6 showed no change or worsening in mood after sleep restriction. Baseline pontine Cho levels distinguished subsequent responders from nonresponders to sleep restriction among depressed participants (z = 2.61, p = 0.008). LIMITATIONS: A limitation of this study is the relatively small sample size. CONCLUSION: Sleep restriction altered levels of pontine tCr and prefrontal Cho in both groups combined, suggesting effects on phospholipid and creatine metabolism. Baseline levels of pontine Cho were linked to subsequent mood responses to sleep loss, suggesting a role for pontine phospholipid metabolism in mood effects of sleep restriction. [ABSTRACT FROM AUTHOR]

Deurveilher S, Cumyn EM, Peers T, Rusak B, Semba K. Estradiol replacement enhances sleep deprivation-induced c-Fos immunoreactivity in forebrain arousal regions of ovariectomized rats. Am J Physiol Regul Integr Comp Physiol 295: RI 328-RI 340, 2008. First published August 27, 2008; doi: 10.1 152/ajpregu.90576.2008.-To understand how female sex hormones influence homeostatic mechanisms of sleep, we studied the effects of estradiol (E[sub2]) replacement on c-Fos immunoreactivity in sleep! wake-regulatory brain areas after sleep deprivation (SD) in ovariectomized rats. Adult rats were ovariectomized and implanted subcutaneously with capsules containing 1713-E[sub2] (10.5 μg; to mimic diestrous E[sub2] levels) or oil. After 2 wk, animals with E[sub2] capsules received a single subcutaneous injection of 17β-E[sub2] (10 μg/kg; to achieve proestrous E[sub2] levels) or oil; control animals with oil capsules received an oil injection. Twenty-four hours later, animals were either left undisturbed or sleep deprived by "gentle handling" for 6 h during the early light phase, and killed. E[sub2] treatment increased serum E[sub2] levels and uterus weights dose dependently, while attenuating body weight gain. Regardless of hormonal conditions, SD increased c-Fos immunoreactivity in all four arousalpromoting areas and four limbic and neuroendocrine nuclei studied, whereas it decreased c-Fos labeling in the sleep-promoting ventrolateral preoptic nucleus (VLPO). Low and high E[sub2] treatments enhanced the SD-induced c-Fos immunoreactivity in the laterodorsal subnucleus of the bed nucleus of stria terminalis and the tuberomammillary nucleus, and in orexin-containing hypothalamic neurons, with no effect on the basal forebrain and locus coeruleus. The high E[sub2] treatment decreased c-Fos labeling in the VLPO under nondeprived conditions. These results indicate that E[sub2] replacement modulates SD-induced or spontaneous c-Fos expression in sleep!wake-regulatory and limbic forebrain nuclei. These modulatory effects of E[sub2] replacement on neuronal activity may be, in part, responsible for E[sub2]'s influence on sleep!wake behavior. [ABSTRACT FROM AUTHOR]

Presents experiments that extend previous studies of how pigeon's memory for the duration of events is affected by the length of the delay and intertrial intervals. Work of Spetch & Rusak (1989); Role of temporal context in regulating memory forduration; Use of standard two-key and three-key pigeon chambers; Choice behavior; Study methods and results.

Discusses research into the effect of exposure of rats and hamsters to light pulses at those phases of the circadian rhythm when light can shift the rhythm. Increased immunoreactivity; Increased messenger RNA; Results.

The effects on activity rhythms of a daily 30 min opportunity to leave the home cage and hoard seeds from an open field were assessed in Syrian hamsters housed in continuous dim illumination. Six of ten hamsters responded with clear entrainment of their activity rhythms to the hoarding opportunity, as demonstrated by responses to phase shifts and by the onset phase of subsequent freerunning rhythms. No entrainable component separate from the freerunning rhythm was ever observed. Two hamsters showed phase shifts in response to the hoarding opportunity, but they did not meet the criteria for stable entrainment, and two did not respond with noticeable changes in rhythmicity. Ablations of the suprachiasmatic nuclei (SCN) were attempted in three hamsters that had entrained stably to the hoarding time. The effects of partial lesions in two animals indicated that the entrained rhythm was controlled by the light-entrainable pacemaker represented by the SCN. The one animal with an apparently complete lesion, however, developed a clear, but irregular, increase in activity in anticipation of the daily hoarding time. SCN ablation apparently unmasked an oscillator system separate from the SCN and susceptible to entrainment by a nonphotic cue. The oscillator mechanism affected by daily hoarding opportunities in hamsters appears to be tightly coupled to the SCN pacemaker, in contrast to the system in rats that is synchronized by daily feeding schedules. [ABSTRACT FROM AUTHOR]