186,361 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
Get PDFSleep 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
No full textThe effect of social stimuli on the accumulation of sleep debt and need for recovery: does copulatory activity increase slow-wave sleep?
No full textEarly life origin of adult insomnia: does prenatal-postnatal stress play a role?
No full textInsomnia is very common in the adult population and it includes a wide spectrum of sequelae, that is, neuroendocrine and cardiovascular alterations as well as psychiatric and neurodegenerative disorders. According to the conceptualization of insomnia in the context of the 3-P model, the importance of predisposing, precipitating, and perpetuating factors has been stressed. Predisposing factors are present before insomnia is manifested and they are hypothesized to interact with precipitating factors, such as environmental stressful events, contributing to the onset of insomnia. Understanding the early-life origins of insomnia may be particularly useful in order to prevent and treat this costly phenomenon. Based on recent evidence, prenatal-early-life stress exposure results in a series of responses that involve the stress system in the child and could persist into adulthood. This may encompass an activation of the hypothalamic-pituitary-adrenal axis accompanied by long-lasting modifications in stress reactivity. Furthermore, early-life stress exposure might play an important role in predisposing to a vulnerability to hyperarousal reactions to negative life events in the adult contributing to the development of chronic insomnia. Epigenetic mechanisms may also be involved in the development of maladaptive stress responses in the newborn, ultimately predisposing to develop a variety of (psycho-) pathological states in adult life
Forced desynchrony of circadian rhythms of body temperature and activity in rats
No full textThe daily rhythm in body temperature is thought to be the result of the direct effects of activity and the effects of an endogenous circadian clock. Forced desynchrony (FD) is a tool used in human circadian rhythm research to disentangle endogenous and activity-related effects on daily rhythms. In the present study, we applied an FD protocol to rats. We subjected 8 rats for 5 days to a 20h forced activity cycle consisting of 10h of forced wakefulness and 10h for rest and sleep. The procedure aimed to introduce a 10h sleep/ 10h wake cycle, which period was different from the endogenous circadian (about 24h) rhythm. Of the variation in the raw body temperature data, 68-77% could be explained by a summation of estimated endogenous circadian cycle and forced activity cycle components of body temperature. Free-running circadian periods of body temperature during FD were similar to free-running periods measured in constant conditions. The applied forced activity cycle reduced clock-related circadian modulation of activity. This reduction of circadian modulation of activity did not affect body temperature. Also, the effects of the forced activity on body temperature were remarkably small
Aggressive and Sexual Social Stimuli Do Not Phase Shift the Circadian Temperature Rhythm in Rats
No full textThe objective of the present study was to determine whether the rat circadian system is sensitive to social stimuli. Male rats were subjected to a sociosexual interaction with an estrous female or to an aggressive interaction with a dominant male conspecific. The interactions lasted for 1h and took place in the middle of the circadian resting phase. Control animals were picked up and handled for a few minutes, but were otherwise left undisturbed. Animals were housed under constant dim red light during the whole period of the experiment. To assess the effects of the interactions on free-running circadian rhythmicity, body temperature was measured by means of radio telemetry. Neither the sociosexual interaction with a female nor the aggressive interaction with another male induced phase shifts or changes in the free-running period. The rat circadian system does not seem to be sensitive to social stimuli directly. Moreover, the finding that aggressive interactions do not phase shift circadian rhythms indicates that the endogenous pacemaker in rats is not sensitive to stressors.
Too Little Sleep Gradually Desensitizes the Serotonin 1A Receptor System
No full textStudy Objectives: In our 24-hour society, frequently disrupted and restricted sleep is a rapidly increasing problem that may contribute to the development of diseases such as depression. One of the proposed neurobiological mechanisms underlying depression is a disturbance in the brain’s serotonergic neurotransmission, particularly a desensitization of the serotonin (5-HT)1A receptor system. However, a relationship between chronic sleep loss and changes in 5-HT1A receptors has not been established yet. Therefore, in the present study, we experimentally tested the hypothesis that chronic sleep restriction leads to desensitization of the 5-HT1A receptor system.
Design: Rats were subjected to a schedule of restricted sleep allowing them 4 hours of sleep per day. Sleep restriction was achieved by placing the animals in slowly rotating wheels. The sensitivity of the 5-HT1A receptor system was examined by measuring the hypothermic response to a standard injection of a 1A agonist.
Results: After 2 days of restricted sleep, the sensitivity of the 5-HT1A receptor system was not yet affected; however, after 8 days of sleep restriction, it was desensitized. Control experiments indicated that the effect of sleep restriction was not due to forced activity or stress. Importantly, the desensitization of the 5-HT1A system persisted for many days even with unlimited recovery sleep. Normalization occurred gradually but required at least 7 days.
Conclusions: Chronic sleep restriction causes a gradual and persistent desensitization of the 5-HT1A receptor system. This finding provides a link between chronic sleep loss and sensitivity for disorders that are associated with altered serotonergic neurotransmission.
Chronic social defeat stress suppresses locomotor activity but does not affect the free-running circadian period of the activity rhythm in mice
Get PDFIn mammals, daily rhythms in behavior and physiology are under control of an endogenous clock or pacemaker located in the suprachiasmatic nucleus (SCN) of the hypothalamus. The SCN assures an optimal temporal organization of internal physiological process and also synchronizes rhythms in physiology and behavior to the cyclic environment. The SCN receives direct light input from the retina, which is capable of resetting the master clock and thereby synchronizes internally driven rhythms to the external light-dark cycle. In keeping with its function as a clock and pacemaker, the SCN appears to be well buffered against influences by other stimuli and conditions that contain no relevant timing information, such as acute stressors. On the other hand, it has been suggested that chronic forms of stress may have gradually accumulating effects that can disturb normal clock function and thereby contribute to stress-related disorders. Therefore, in the present study we investigated whether chronic intermittent social stress affects the endogenous period and phase of the free-running activity rhythm in mice. Adult male mice were maintained in constant dim red light conditions and exposed to a daily 20 min social defeat stress session for 10 consecutive days, either during the first half of their activity phase or the first half of their resting phase. The overall amount of running wheel activity was strongly suppressed during the 10 days of social defeat, to about 50% of the activity in non-defeated control mice. Activity levels gradually normalized during post-defeat recovery days. Despite the strong suppression of activity in defeated animals, the endogenous free-running circadian period of the activity rhythm and the phase of activity onset were not affected. These findings are thus in agreement with earlier studies suggesting that the circadian pacemaker in the SCN that is driving the rhythmicity in activity is well-protected against stress. Even severe social defeat stress for 10 consecutive days, which has a major effect on the levels of activity, does not affect the pace of the endogenous clock. Keywords: Stress disorders, Chronic stress, Social conflict, Suprachiasmatic nucleus, Circadian rhythms, Daily rhythms, Activity patterns, Rhythm disturbanc
Behavioural and Physiological Consequences of a Single Social Defeat in Roman High- and Low-Avoidance Rats
No full textThe behavioural and physiological consequences of a single social defeat were studied in Roman high-avoidance (RHA) and Roman low-avoidance (RLA) rats, two rat lines with a genetically determined difference in the way of responding to or coping with stressors. Animals were subjected to social defeat by placing them in the cage of an aggressive male conspecific for 1 h. In both RHA and RLA rats, social defeat induced a profound increase in body temperature during the circadian resting phase, lasting for up to 10 days after the conflict. The increase in resting temperature was paralleled by a slight decrease in spontaneous home cage activity. Food intake and growth were suppressed for a number of days, resulting in a long-lasting lower body weight compared to non-stressed control animals. An open field test 2 days after defeat showed a social stress-induced decrease in locomotion in a novel environment. Despite the well-known differentiation between RHA and RLA rats in their behavioural and neuroendocrine response pattern to acute environmental challenges, the present study did not show major differences in the long-term consequences of social defeat.
Social stress in rats: An animal model of depression?
No full textOur current understanding of the physiological mechanisms underlying depressive disorders is not only based on behavioral, neuroendocrine and pharmacological studies in depressed humans, but also on experimental studies in a wide variety of animal models of depression. Ideally, the two approaches should operate in close interaction, each providing additional information to the other approach. However, in practice the animal model approach seems to be rather independent from the human studies. In a critical evaluation of the available animal models of depression, Willner concluded that none of the models fulfilled the criteria of a sufficient face, construct and predictive validity. Although this evaluation was made ten years ago, we feel that the situation has improved very little since that time. Most animal models fail to sufficiently mimic both the etiology and the symptomatology of human depressive disorders. With respect to the etiology, stress and major life events are generally considered to be an important factor in the development of depression. Most of the animal models however use stressors which bear little or no relationship to the biology of the species, i.e. to the situations an animal may meet in its everyday life in a natural habitat. Moreover, these models do not pay attention to the temporal dynamics of the disease. In humans, the disease is characterized by its gradual onset, which is often preceded by symptoms of anxiety. Moreover, a relatively large number of patients suffers from recurrent episodes of depression, which tend to occur with decreasing intervals and increasing duration and severity. If we want to improve our knowledge of the causal mechanisms of depression, animal models which allow an experimental analysis of the temporal dynamics of the disease are essential
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