Effect of melatonin supplementation upon parental care and nestling growth in arctic-breeding songbirds.

Arctic-breeding birds exhibit around-the-clock activity, and these activity cycles are postulated to maximize reproductive success during the short breeding season characteristic of high-latitude regions. Two closely related species of arctic-breeding songbirds, Lapland longspurs (Calcarius lapponicus; ground-nesting) and snow buntings (Plectrophenax nivalis; cavity-nesting) exhibit extended activity cycles throughout the polar day (71° N) except for 4-5 h of daily quiescence. Ground-nesting Lapland longspurs experience higher levels of nest predation than cavity-nesting snow buntings, and this difference is reflected in elevated nest vigilance in male longspurs compared with snow buntings.

Effect of glucocorticoid blockade on inflammatory responses to acute sleep fragmentation in male mice.

The association between sleep and the immune-endocrine system is well recognized, but the nature of that relationship is not well understood. Sleep fragmentation induces a pro-inflammatory response in peripheral tissues and brain, but it also activates the hypothalamic-pituitary-adrenal (HPA) axis, releasing glucocorticoids (GCs) (cortisol in humans and corticosterone in mice). It is unclear whether this rapid release of glucocorticoids acts to potentiate or dampen the inflammatory response in the short term.

Temporal dynamics of pro-inflammatory cytokines and serum corticosterone following acute sleep fragmentation in male mice.

Obstructive sleep apnea is increasing worldwide, leading to disordered sleep patterns and inflammatory responses in brain and peripheral tissues that predispose individuals to chronic disease. Pro-inflammatory cytokines activate the inflammatory response and are normally regulated by glucocorticoids secreted from adrenal glands. However, the temporal dynamics of inflammatory responses and hypothalamic-pituitary-adrenal (HPA) axis activation in relation to acute sleep fragmentation (ASF) are undescribed.

Inflammation from Sleep Fragmentation Starts in the Periphery Rather than Brain in Male Mice.

Obstructive sleep apnea is increasing worldwide, leading to disordered sleep patterns and inflammatory responses in brain and peripheral tissues that predispose individuals to chronic disease. Pro-inflammatory cytokines activate the inflammatory response and are normally regulated by glucocorticoids secreted from adrenal glands. However, the temporal dynamics of inflammatory responses and hypothalamic-pituitary-adrenal (HPA) axis activation in relation to acute sleep fragmentation (ASF) are undescribed.

Peripheral Sympathectomy Alters Neuroinflammatory and Microglial Responses to Sleep Fragmentation in Female Mice.

Sleep loss, either induced by obstructive sleep apnea or other forms of sleep dysfunction, induces an inflammatory response, as commonly measured by increased circulating levels of pro-inflammatory cytokines. Increased catecholamines from sympathetic nervous system (SNS) activation regulates this peripheral inflammation. However, the role that catecholamines play in mediating neuroinflammation from sleep perturbations is undescribed.

Contrasting effects of sleep fragmentation and angiotensin-II treatment upon pro-inflammatory responses of mice.

Disordered sleep promotes inflammation in brain and peripheral tissues, but the mechanisms that regulate these responses are poorly understood. One hypothesis is that activation of the sympathetic nervous system (SNS) from sleep loss elevates blood pressure to promote vascular sheer stress leading to inflammation. As catecholamines produced from SNS activation can directly regulate inflammation, we pharmacologically altered blood pressure using an alternative approach-manipulation of the renin-angiotensin system (RAS).

Alpha- and beta- adrenergic receptors regulate inflammatory responses to acute and chronic sleep fragmentation in mice.

Sleep is a recuperative process, and its dysregulation has cognitive, metabolic, and immunological effects that are largely deleterious to human health. Epidemiological and empirical studies have suggested that sleep fragmentation (SF) as result of obstructive sleep apnea (OSA) and other sleep abnormalities leads to pronounced inflammatory responses, which are influenced by the sympathetic nervous system (SNS). However, the underlying molecular mechanisms contributing to SNS regulation of SF-induced inflammation are not fully understood.

An anti-narcolepsy drug reveals behavioral and fitness costs of extreme activity cycles in arctic-breeding songbirds.

Sleep loss impairs cognitive function, immunological responses and general well-being in humans. However, sleep requirements in mammals and birds vary dramatically. In circumpolar regions with continuous summer light, daily sleep duration is reduced, particularly in breeding birds.

Effect of sleep loss on executive function and plasma corticosterone levels in an arctic-breeding songbird, the Lapland longspur (Calcarius lapponicus).

Sleep is a fundamental component of vertebrate life, although its exact functions remain unclear. Animals deprived of sleep typically show reduced neurobiological performance, health, and in some cases, survival. However, a number of vertebrate taxa exhibit adaptations that permit normal activities even when sleep is reduced.

Chemical sympathectomy reduces peripheral inflammatory responses to acute and chronic sleep fragmentation.

Sleep loss contributes to the development of cardiovascular, metabolic, and neurological disorders by promoting a systemic proinflammatory phenotype. The neuroendocrine-immune mechanisms contributing to such pathologies are poorly understood. The sympathetic nervous system (SNS) regulates immunity and is often activated following sleep disturbances.

Light at night disrupts diel patterns of cytokine gene expression and endocrine profiles in zebra finch (Taeniopygia guttata).

Increased exposure to light pollution perturbs physiological processes through misalignment of daily rhythms at the cellular and tissue levels. Effects of artificial light-at-night (ALAN) on diel properties of immunity are currently unknown. We therefore tested the effects of ALAN on diel patterns of cytokine gene expression, as well as key hormones involved with the regulation of immunity, in zebra finches (Taeniopygia guttata).

Transcriptomic analysis of immune response to bacterial lipopolysaccharide in zebra finch (Taeniopygia guttata).

Background: Despite the convergence of rapid technological advances in genomics and the maturing field of ecoimmunology, our understanding of the genes that regulate immunity in wild populations is still nascent. Previous work to assess immune function has relied upon relatively crude measures of immunocompetence. However, with next-generation RNA-sequencing, it is now possible to create a profile of gene expression in response to an immune challenge.

Short-Term Sleep Loss Alters Cytokine Gene Expression in Brain and Peripheral Tissues and Increases Plasma Corticosterone of Zebra Finch (Taeniopygia guttata).

Lack of sleep incurs physiological costs that include increased inflammation and alterations in the hypothalamic-pituitary-adrenal axis. Specifically, sleep restriction or deprivation leads to increased pro-inflammatory cytokine expression and elevated glucocorticoids in rodent models, but whether birds exact similar costs is unknown. In this study, we examined whether zebra finch (Taeniopygia guttata), an avian model species, exhibits physiological costs of sleep loss by using a novel automated sleep fragmentation/deprivation method, wherein a horizontal wire sweeps across a test cage to disrupt sleep every 120 s.

Acute sleep fragmentation does not alter pro-inflammatory cytokine gene expression in brain or peripheral tissues of leptin-deficient mice.

Obesity and sleep fragmentation (SF) are often co-occurring pro-inflammatory conditions in patients with obstructive sleep apnea. Leptin is a peptide hormone produced by adipocytes that has anorexigenic effects upon appetite while regulating immunity. The role of leptin in mediating inflammatory responses to SF is incompletely understood.

Neuroendocrine-immune circuits, phenotypes, and interactions.

Multidirectional interactions among the immune, endocrine, and nervous systems have been demonstrated in humans and non-human animal models for many decades by the biomedical community, but ecological and evolutionary perspectives are lacking. Neuroendocrine-immune interactions can be conceptualized using a series of feedback loops, which culminate into distinct neuroendocrine-immune phenotypes. Behavior can exert profound influences on these phenotypes, which can in turn reciprocally modulate behavior.

Novel environment influences the effect of paradoxical sleep deprivation upon brain and peripheral cytokine gene expression.

Sleep loss increases inflammatory mediators in brain and peripheral tissues, but the mechanisms underlying this association are not fully understood. Male C57BL/6j mice were exposed to paradoxical sleep deprivation (PSD) for 24h using the modified multiple platform (MMP) technique (platforms over water) or two different controls: home cage or a dry platform cage, which constituted a novel environment. PSD mice exhibited increased IL-1β and TNF-α pro-inflammatory gene expression in brain (hypothalamus, hippocampus, pre-frontal cortex), as well as in peripheral tissues (liver, spleen), when compared with home-cage controls.

Acute sleep fragmentation induces tissue-specific changes in cytokine gene expression and increases serum corticosterone concentration.

Sleep deprivation induces acute inflammation and increased glucocorticosteroids in vertebrates, but effects from fragmented, or intermittent, sleep are poorly understood. Considering the latter is more representative of sleep apnea in humans, we investigated changes in proinflammatory (IL-1β, TNF-α) and anti-inflammatory (TGF-β1) cytokine gene expression in the periphery (liver, spleen, fat, and heart) and brain (hypothalamus, prefrontal cortex, and hippocampus) of a murine model exposed to varying intensities of sleep fragmentation (SF). Additionally, serum corticosterone was assessed.

Revealing a circadian clock in captive arctic-breeding songbirds, lapland longspurs (Calcarius lapponicus), under constant illumination.

Most organisms in temperate or tropic regions employ the light-dark (LD) cycle as the primary Zeitgeber to synchronize circadian rhythms. At higher latitudes (>66°33'), continuous illumination during the summer presents a significant time-keeping dilemma for polar-adapted species. Lapland longspurs (Calcarius lapponicus), arctic-breeding migratory songbirds, are one of the few recorded species maintaining an intact diel rhythm in activity and plasma melatonin titers during polar summer.

Sleep deprivation attenuates endotoxin-induced cytokine gene expression independent of day length and circulating cortisol in male Siberian hamsters (Phodopus sungorus).

Sleep is restorative, whereas reduced sleep leads to negative health outcomes, such as increased susceptibility to disease. Sleep deprivation tends to attenuate inflammatory responses triggered by infection or exposure to endotoxin, such as bacterial lipopolysaccharide (LPS). Previous studies have demonstrated that Siberian hamsters (Phodopus sungorus), photoperiodic rodents, attenuate LPS-induced fever, sickness behavior and upstream pro-inflammatory gene expression when adapted to short day lengths.

Keeping time under the midnight sun: behavioral and plasma melatonin profiles of free-living Lapland longspurs (Calcarius lapponicus) during the arctic summer.

Polar environments are characterized by discrete periods of continuous light or darkness during the summer and winter months, respectively. Because the light/dark cycle serves as the primary Zeitgeber to synchronize rhythms of most organisms, its seasonal absence in polar regions poses challenges to the circadian organization of organisms that reside in these environments. Although some species become arrhythmic, others, such as migratory songbirds, are able to maintain an intact diurnal rhythm during polar summer.

Photoperiod alters duration and intensity of non-rapid eye movement sleep following immune challenge in Siberian hamsters (Phodopus sungorus).

Sleep is regulated by circadian and homeostatic processes, but can be altered by infectious disease. During infection or exposure to inflammatory stimuli, such as bacterial lipopolysaccharide (LPS), the duration and intensity of non-rapid eye movement sleep (NREMS), as measured by electoencephalogram (EEG) delta waves (.5-4 Hz), increase.

Testosterone treatment diminishes sickness behavior in male songbirds.

Males of many vertebrate species are typically more prone to disease and infection than female conspecifics, and this sexual difference is partially influenced by the immunosuppressive properties of testosterone (T) in males. T-induced immunosuppression has traditionally been viewed as a pleiotropic handicap, rather than an adaptation. Recently, it has been hypothesized that suppression of sickness behavior, or the symptoms of infection, may have adaptive value if sickness interferes with the expression of T-mediated behaviors important for male reproductive success.