No loss of orexin/hypocretin, melanin-concentrating hormone or locus coeruleus noradrenergic neurons in a rat model of chronic sleep restriction.

Chronic sleep restriction (CSR) is common in modern society, adversely affecting cognitive performance and health. Yet how it impacts neurons regulating sleep remains unclear. Several studies using mice reported substantial losses of wake-active orexin/hypocretin and locus coeruleus (LC) noradrenergic neurons, but not rapid eye movement sleep-active melanin-concentrating hormone (MCH) neurons, following CSR.

Homeostatic sleep and body temperature responses to acute sleep deprivation are preserved following chronic sleep restriction in rats.

Chronic sleep insufficiency is common in our society and has negative cognitive and health impacts. It can also alter sleep regulation, yet whether it affects subsequent homeostatic responses to acute sleep loss is unclear. We assessed sleep and thermoregulatory responses to acute sleep deprivation before and after a '3/1' chronic sleep restriction protocol in adult male Wistar rats.

Microglia dynamics in sleep/wake states and in response to sleep loss.

Sleep has an essential role for optimal brain function, but the cellular substrates for sleep regulation are not fully understood. Microglia, the immune cells of the brain, have gained increasingly more attention over the last two decades for their important roles in various brain functions that extend beyond their well-known immune function, including brain development, neuronal protection, and synaptic plasticity. Here we review recent advances in understanding: i) morphological and phenotypic dynamics of microglia including process motility/growth and gene/protein expression, and ii) microglia-neuron interactions including phagocytosis and contact at synapses which alters neuronal circuit activity, both under physiological state in the adult brain.

Altered circadian activity and sleep/wake rhythms in the stable tubule only polypeptide (STOP) null mouse model of schizophrenia.

Sleep and circadian rhythm disruptions commonly occur in individuals with schizophrenia. Stable tubule only polypeptide (STOP) knockout (KO) mice show behavioral impairments resembling symptoms of schizophrenia. We previously reported that STOP KO mice slept less and had more fragmented sleep and waking than wild-type littermates under a light/dark (LD) cycle.

Homeostatic state of microglia in a rat model of chronic sleep restriction.

Chronic sleep restriction (CSR) negatively impacts brain functions. Whether microglia, the brain's resident immune cells, play any role is unknown. We studied microglia responses to CSR using a rat model featuring slowly rotating wheels (3 h on/1 h off), which was previously shown to induce both homeostatic and adaptive responses in sleep and attention.

Sex differences in age-related changes in the sleep-wake cycle.

Age-related changes in sleep and circadian regulation occur as early as the middle years of life. Research also suggests that sleep and circadian rhythms are regulated differently between women and men. However, does sleep and circadian rhythms regulation age similarly in men and women? In this review, we present the mechanisms underlying age-related differences in sleep and the current state of knowledge on how they interact with sex.

Region-specific increases in FosB/ΔFosB immunoreactivity in the rat brain in response to chronic sleep restriction.

Using a rat model of chronic sleep restriction (CSR) featuring periodic sleep deprivation with slowly rotating wheels (3h on/1h off), we previously observed that 99h of this protocol induced both homeostatic and allostatic (adaptive) changes in physiological and behavioural measures. Notably, the initial changes in sleep intensity and attention performance gradually adapted during CSR despite accumulating sleep loss. To identify brain regions involved in these responses, we used FosB/ΔFosB immunohistochemistry as a marker of chronic neuronal activation.

Disruptions of Sleep/Wake Patterns in the Stable Tubule Only Polypeptide (STOP) Null Mouse Model of Schizophrenia.

Disruption of sleep/wake cycles is common in patients with schizophrenia and correlates with cognitive and affective abnormalities. Mice deficient in stable tubule only polypeptide (STOP) show cognitive, behavioral, and neurobiological deficits that resemble those seen in patients with schizophrenia, but little is known about their sleep phenotype. We characterized baseline sleep/wake patterns and recovery sleep following sleep deprivation in STOP null mice.

Psychomotor vigilance task performance during and following chronic sleep restriction in rats.

Study Objectives: Chronic sleep restriction (CSR) impairs sustained attention in humans, as commonly assessed with the psychomotor vigilance task (PVT). To further investigate the mechanisms underlying performance deficits during CSR, we examined the effect of CSR on performance on a rat version of PVT (rPVT).

Design: Adult male rats were trained on a rPVT that required them to press a bar when they detected irregularly presented, brief light stimuli, and were then tested during CSR.

Social and environmental contexts modulate sleep deprivation-induced c-Fos activation in rats.

People often sleep deprive themselves voluntarily for social and lifestyle reasons. Animals also appear to stay awake longer as a result of their natural curiosity to explore novel environments and interact socially with conspecifics. Although multiple arousal systems in the brain are known to act jointly to promote and maintain wakefulness, it remains unclear whether these systems are similarly engaged during voluntary vs.

Ovarian hormones promote recovery from sleep deprivation by increasing sleep intensity in middle-aged ovariectomized rats.

Sleep disturbances are commonly associated with menopause. Hormone replacement therapy is often used to treat various menopausal symptoms, but its efficacy for improving sleep is a matter of debate. We addressed this question by using a rodent model of ovarian hormone loss and replacement in midlife.

Estradiol treatment modulates spontaneous sleep and recovery after sleep deprivation in castrated male rats.

Exogenous estradiol (E) is used occasionally to treat the side effects associated with androgen-deprivation in men, but its effects on sleep patterns have received little attention. We examined whether E modulates sleep patterns and recovery from sleep loss in castrated male rats. Adult male rats were castrated and implanted subcutaneously with Silastic tubes containing either oil (Cast+Oil) or E (Cast+E).

Behavioural and neuronal activation after microinjections of AMPA and NMDA into the perifornical lateral hypothalamus in rats.

The perifornical lateral hypothalamic area (PeFLH), which houses orexin/hypocretin (OX) neurons, is thought to play an important role in arousal, feeding, and locomotor activity. The present study examined behavioural effects of activating PeFLH neurons with microinjections of ionotropic glutamate receptor agonists. Three separate unilateral microinjections of either (1) AMPA (1 and 2mM in 0.

Female reproductive hormones alter sleep architecture in ovariectomized rats.

Study Objectives: Treating ovariectomized rats with physiological levels of estradiol and/or progesterone affects aspects of both baseline (24 h) sleep and recovery (18 h) sleep after 6 h of sleep deprivation. We have extended the analysis of these effects by examining several additional parameters of sleep architecture using the same data set as in our previous study (Deurveilher et al. SLEEP 2009;32(7):865-877).

Role of polysialylated neural cell adhesion molecule in rapid eye movement sleep regulation in rats.

Recent evidence suggests that synaptic plasticity occurs during homeostatic processes, including sleep-wakefulness regulation, although the underlying mechanisms are not well understood. Polysialylated neural cell adhesion molecule (PSA NCAM) is a transmembrane protein that has been implicated in various forms of plasticity. To investigate whether PSA NCAM is involved in the neuronal plasticity associated with spontaneous sleep-wakefulness regulation and sleep homeostasis, four studies were conducted using rats.

Estradiol and progesterone modulate spontaneous sleep patterns and recovery from sleep deprivation in ovariectomized rats.

Study Objectives: Women undergo hormonal changes both naturally during their lives and as a result of sex hormone treatments. The objective of this study was to gain more knowledge about how these hormones affect sleep and responses to sleep loss.

Design: Rats were ovariectomized and implanted subcutaneously with Silastic capsules containing oil vehicle, 17 beta-estradiol and/or progesterone.

Transforming growth factor-alpha and glial fibrillary acidic protein in the hamster circadian system: daily profile and cellular localization.

Transforming growth factor-alpha (TGF-alpha) has been identified as a potential output signal of the principal circadian pacemaker housed in the mammalian suprachiasmatic nucleus (SCN). The goal of the present study was to characterize the temporal pattern and cellular localization of TGF-alpha immunoreactivity (IR), and to examine its localization relative to astrocytic and neuronal markers in the hamster circadian system. In contrast to previous reports of circadian rhythms in TGF-alpha mRNA levels in the hamster SCN, we did not detect any statistically significant changes in the levels of TGF-alpha protein IR in the hamster SCN across a 14:10 light-dark cycle using densitometric analyses.

Differential c-Fos immunoreactivity in arousal-promoting cell groups following systemic administration of caffeine in rats.

Despite the widespread use of caffeine, the neuronal mechanisms underlying its stimulatory effects are not completely understood. By using c-Fos immunohistochemistry as a marker of neuronal activation, we recently showed that stimulant doses of caffeine activate arousal-promoting hypothalamic orexin (hypocretin) neurons. In the present study, we investigated whether other key neurons of the arousal system are also activated by caffeine, via dual immunostaining for c-Fos and transmitter markers.

Indirect projections from the suprachiasmatic nucleus to the median preoptic nucleus in rat.

We recently showed, using dual tract-tracing, that the suprachiasmatic nucleus (SCN), the site of the principal circadian clock in mammals, may have indirect projections to the sleep-promoting ventrolateral preoptic nucleus (VLPO) via relays in the medial preoptic area (MPA), dorsomedial hypothalamic nucleus (DMH), and, to a lesser extent, the subparaventricular zone (SPVZ). Here, we found that the injection of the rostral MPA, the periventricular nucleus/medial SPVZ, and the caudal DMH with a mixture of anterograde and retrograde tracers resulted in dense anterograde labeling in the median preoptic nucleus (MnPO), another key sleep-promoting nucleus in the preoptic region. The retrograde labeling in the SCN was evident as previously reported.

The cholinesterase inhibitor DFP facilitates the expression of paradoxical sleep (PS) propensity in rats subjected to short-term PS deprivation.

Short-term paradoxical sleep (PS) deprivation was used to examine the effects of chronic exposure to subtoxic doses of the cholinesterase inhibitor diisopropylfluorophosphate (DFP) on PS regulation. Rats were injected once daily with DFP (0.2 mg/kg per day; s.

Indirect projections from the suprachiasmatic nucleus to the ventrolateral preoptic nucleus: a dual tract-tracing study in rat.

The suprachiasmatic nucleus (SCN) contains a master clock for most circadian rhythms in mammals, including daily sleep-wake cycles. The ventrolateral preoptic nucleus (VLPO) plays a key role in sleep generation and, as such, might be an important target of the SCN circadian signal. However, direct SCN projections to the VLPO are limited, suggesting that most of the SCN output to the VLPO might be conveyed indirectly.