25,893 research outputs found
Effects of social stimuli on sleep in mice: non-rapid-eye-movement (NREM) sleep is promoted by aggressive interaction but not by sexual interaction
Full text linkSleep is generally considered to be a process of recovery from prior wakefulness. In addition to being affected by the duration of the waking period, sleep architecture and sleep EEG also depend on the quality of wakefulness. In the present experiment, we examined how sleep is affected by different social stimuli (social conflict and sexual interaction). Male C57BL/6J mice were placed in the cage of an aggressive dominant male or an estrous female for 1 h in the middle of the light phase. The conflict with an aggressive male had a pronounced NREM sleep-promoting effect. EEG slow wave activity, a measure of NREM sleep intensity, was increased for about 6 h and NREM sleep time was significantly increased for 12 h. REM sleep was strongly suppressed during the remainder of the light phase after the conflict, followed by a rebound later in the recovery phase. The sexual interaction, in contrast, had only mild effects. Both NREM sleep and REM sleep were somewhat suppressed shortly after the interaction. In a separate group of mice, blood samples were taken to measure prolactin and corticosterone. The results suggest that the temporary suppression of REM sleep following the social stimuli may be partly due to elevated corticosterone. The different effects of the social stimuli on NREM sleep are not easily explained by differences in the hormone responses. In conclusion, although both social conflict and sexual interaction induce a strong physiological activation, only social conflict has a strong stimulatory effect on NREM sleep mechanisms.
Animal Models of Social Stress: Implications for the Study of Stress Related Pathologies in Humans
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Animal studies on the role of sleep in memory:From behavioral performance to molecular mechanisms
No full textAlthough the exact functions of sleep remain a topic of debate, several hypotheses propose that sleep benefits neuronal plasticity, which ultimately supports brain function and cognition. For over a century, researchers have applied a wide variety of behavioral, electrophysiological, biochemical and molecular approaches to study how memory processes are promoted by sleep and perturbed by sleep loss. Interestingly, experimental studies indicate that cognitive impairments as a consequence of sleep deprivation appear to be most severe with learning and memory processes that require the hippocampus, which suggests that this brain region is particularly sensitive to the consequences of sleep loss. Moreover, recent studies in laboratory rodents indicate that sleep deprivation impairs hippocampal neuronal plasticity and memory processes by attenuating intracellular cyclic adenosine monophosphate (cAMP) - protein kinase A (PKA) signaling. Attenuated cAMP-PKA signaling can lead to a reduced activity of the transcription factor cAMP response element binding protein (CREB) and ultimately affect the expression of genes and proteins involved in neuronal plasticity and memory formation. Pharmacogenetic experiments in mice show that memory deficits following sleep deprivation can be prevented by specifically boosting cAMP signaling in excitatory neurons of the hippocampus. Given the high incidence of sleep disturbance and sleep restriction in our 24/7 society, understanding the consequences of sleep loss and unraveling the underlying molecular mechanisms is of great importance
Chronically restricted or disrupted sleep as a causal factor in the development of depression
No full textSleep problems are a common complaint in the majority of people suffering from depression. While sleep complaints were traditionally seen as a symptom of mood disorders, accumulating evidence suggests that in many cases the relationship may be reverse as well. A long list of longitudinal studies shows that sleep complaints often precede the onset of depression and constitute an independent risk factor for the development of the disorder. Additionally, experimental studies in animals show that chronically restricted or disrupted sleep may gradually induce neurobiological changes that are very similar to what has been reported for depressed patients. The mechanisms through which insufficient sleep increases the risk for depression are poorly understood but may include effects of sleep disturbance on neuroendocrine stress systems, serotonergic neurotransmission, and various interacting signaling pathways involved in the regulation of neuronal plasticity and neurogenesis. Because sleep is considered to play a crucial role in regulating neuronal plasticity and synaptic strength, chronically insufficient sleep may contribute to depression through an impairment of these plasticity processes leading to altered connectivity and communication within and between brain regions involved in the regulation of mood.</p
Stress, arousal, and sleep
No full textStress is considered to be an important cause of disrupted sleep and insomnia. However, controlled and experimental studies in rodents indicate that effects of stress on sleep-wake regulation are complex and may strongly depend on the nature of the stressor. While most stressors are associated with at least a brief period of arousal and wakefulness, the subsequent amount and architecture of recovery sleep can vary dramatically across conditions even though classical markers of acute stress such as corticosterone are virtually the same. Sleep after stress appears to be highly influenced by situational variables including whether the stressor was controllable and/or predictable, whether the individual had the possibility to learn and adapt, and by the relative resilience and vulnerability of the individual experiencing stress. There are multiple brain regions and neurochemical systems linking stress and sleep, and the specific balance and interactions between these systems may ultimately determine the alterations in sleep-wake architecture. Factors that appear to play an important role in stress-induced wakefulness and sleep changes include various monominergic neurotransmitters, hypocretins, corticotropin releasing factor, and prolactin. In addition to the brain regions directly involved in stress responses such as the hypothalamus, the locus coeruleus, and the amygdala, differential effects of stressor controllability on behavior and sleep may be mediated by the medial prefrontal cortex. These various brain regions interact and influence each other and in turn affect the activity of sleep-wake controlling centers in the brain. Also, these regions likely play significant roles in memory processes and participate in the way stressful memories may affect arousal and sleep. Finally, stress-induced changes in sleep-architecture may affect sleep-related neuronal plasticity processes and thereby contribute to cognitive dysfunction and psychiatric disorders.</p
Author Peter FitzSimons speaking at the National Library of Australia, Canberra, 13 November 2012 /
No full textTitle from acquisitions documentation.; Part of the collection: Portraits of author Peter FitzSimons speaking at the National Library of Australia, Canberra, 13 November 2012.; Acquired in digital format; access copy available online.; Mode of access: Online.; Photographed by a staff member of the National Library of Australia
The effects of social defeat and other stressors on the expression of circadian rhythms
No full textMost biological functions display a 24 h rhythm that, in mammals, is under the control of an endogenous circadian oscillator located in the suprachiasmatic nuclei (SCN) of the hypothalamus. The circadian system provides an optimal temporal organization for physiological processes and behavior in relation to a cyclic environment imposed upon organisms by the regular alternation of day and night. In line with its function as a clock that serves to maintain a stable phase-relationship between endogenous rhythms and the light-dark cycle, the circadian oscillator appears to be well protected against unpredictable stressful stimuli. Available data do not provide convincing evidence that stress is capable of perturbing the central circadian oscillator in the SCN. However, the shape and amplitude of a rhythm is not determined exclusively by the SCN and certain stressors can strongly affect the output of the clock and the expression of the rhythms. In particular, social stress in rodents has been found to cause severe disruptions of the body temperature, heart rate and locomotor activity rhythms, especially in animals that are subject to uncontrollable stress associated with defeat and subordination. Such rhythm disturbances may be due to effects of stress on sub-oscillators that are known to exist in many tissues, which are normally under the control of the SCN, or due to other effects of stress that mask the output of the circadian system. These disturbances of peripheral rhythms represent an imbalance between normally precisely orchestrated physiological and behavioral processes that may have severe consequence for the health and well being of the organism
Sleep and adult neurogenesis:Implications for cognition and mood
No full textThe hippocampal dentate gyrus plays a critical role in learning and memory throughout life, in part by the integration of adult born neurons into existing circuits. Neurogenesis in the adult hippocampus is regulated by numerous environmental, physiological and behavioral factors known to affect learning and memory. Sleep is also important for learning and memory. Here we critically examine evidence from correlation, deprivation, and stimulation studies that sleep may be among those factors that regulate hippocampal neurogenesis. There is mixed evidence for correlations between sleep variables and rates of hippocampal cell proliferation across the day, the year and the lifespan. There is modest evidence that periods of increased sleep are associated with increased cell proliferation or survival. There is strong evidence that disruptions of sleep exceeding 24h, by total deprivation, selective REM sleep deprivation, chronic restriction or fragmentation, significantly inhibit cell proliferation and in some cases neurogenesis. The mechanisms by which sleep disruption inhibits neurogenesis are not fully understood. Although sleep disruption procedures are typically at least mildly stressful, elevated adrenal corticosterone secretion is not necessary for this effect. However, procedures that prevent both elevated corticosterone and interleukin 1 signaling have been found to block the effect of sleep deprivation on cell proliferation. This result suggests that sleep loss impairs hippocampal neurogenesis by the presence of wake-dependent factors, rather than by the absence of sleep-specific processes. This would weigh against a hypothesis that regulation of neurogenesis is a function of sleep. Nonetheless, impaired neurogenesis may underlie some of the memory and mood effects associated with acute and chronic sleep disruptions
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