Repeated social defeat stress induces chronic hyperthermia in rats

Hayashida, Sota; Oka, Takahiro; Mera, Takashi; Tsuji, Sadatoshi

doi:10.1016/j.physbeh.2010.04.027

Cited by 49 publications

(24 citation statements)

References 40 publications

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“…These changes are in line with earlier reports [4,22,23,24,25,26]. The social stress-induced hyperthermia in rats was shown to be mediated through the activation of thermoregulatory sympathetic premotor neurons in the medullary raphe region [27], which has been associated with depressive-like behaviour [28]. In addition, the CRF has been involved in the regulation of daily temperature rhythms [29], and the increase of the activity of the HPA axis and CRF production following a response to stress exposure could be involved in the alterations observed in the temperature variable.…”

Section: Discussionsupporting

confidence: 90%

Simultaneous Changes in Sleep, qEEG, Physiology, Behaviour and Neurochemistry in Rats Exposed to Repeated Social Defeat Stress

Ahnaou

Drinkenburg²

2016

Neuropsychobiology

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Depression is a heterogeneous disorder characterized by alterations at psychological, behavioural, physiological, neurophysiological, and neurochemical levels. Social stress is a prevalent stress in man, and the repeated social defeat stress model in rats has been proposed as being the rodent equivalent to loss of control, which in subordinate animals produces alterations that resemble several of the cardinal symptoms found in depressed patients. Here, rats followed a resident-intruder protocol for 4 consecutive days during which behavioural, physiological, and electroencephalographic (EEG) parameters were simultaneously monitored in subordinate rats. On day 5, prefrontal dopamine (DA) and hippocampal serotonin (5-HT) as well as corticosterone were measured in submissive rats that had visual, acoustic, and olfactory (but no physical) contact with a dominant, resident conspecific rat. Socially defeated rats demonstrated increases in ultrasonic vocalizations (20-25 KHz), freezing, submissive defensive behaviour, inactivity, and haemodynamic response, while decreases were found in repetitive grooming behaviour and body weight. Additionally, alterations in the sleep-wake architecture were associated with reduced active waking, enhanced light sleep, and increased frequency of transitions from light sleep to quiet wakefulness, indicating sleep instability. Moreover, the attenuation of EEG power over the frequency range of 4.2-30 Hz, associated with a sharp transient increase in delta oscillations, appeared to reflect increased brain activity and metabolism in subordinate animals. These EEG changes were synchronous with a marked increase in body temperature and a decrease in locomotor activity. Furthermore, psychosocial stress consistently increased 5-HT, DA, and corticosterone levels.The increased levels of cortical DA and hippocampal 5-HT during social threat may reflect a coping mechanism to promote alertness and psychological adaptation to provocative and threatening stimuli. These neurophysiological changes are hypothesized to be the consequence of dynamics in monoamine systems, which could be useful markers for disease progression in the aetiology of depression.

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Section: Discussionsupporting

confidence: 90%

Simultaneous Changes in Sleep, qEEG, Physiology, Behaviour and Neurochemistry in Rats Exposed to Repeated Social Defeat Stress

Ahnaou

Drinkenburg²

2016

Neuropsychobiology

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“…In many animal models of depression the depressive-like behavior is coincident with changes in body temperature or thermoregulation [31-33]. To examine the relationship between rectal temperature at the end of the swim and immobility during the swim we examined the correlation coefficients between rectal temperature and immobility of mice during each daily swim, but found no significant relationship between these data (data not shown).…”

Section: Resultsmentioning

confidence: 99%

After a cold conditioning swim, UCP2-deficient mice are more able to defend against the cold than wild type mice

Abdelhamid

Kovács

Nunez

et al. 2014

Physiology & Behavior

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Uncoupling protein 2 (UCP2) is widely distributed throughout the body including the brain, adipose tissue and skeletal muscles. In contrast to UCP1, UCP2 does not influence resting body temperature and UCP2-deficient (-/-) mice have normal thermoregulatory responses to a single exposure to cold ambient temperatures. Instead, UCP2-deficient mice are more anxious, exhibit anhedonia and have higher circulating corticosterone than wild type mice. To test the possible role of UCP2 in depressive behavior we exposed UCP2-deficient and wild type mice to a cold (26°C) forced swim and simultaneously measured rectal temperatures during and after the swim. The time that UCP2-deficient mice spent immobile did not differ from wild type mice and all mice floated more on day 2. However, UCP2-deficient mice were more able to defend against the decrease in body temperature during a second daily swim at 26°C than wild type mice (area under the curve for wild type mice: 247.0 ± 6.4; for UCP2-deficient mice: 284.4 ± 3.8, P<0.0001, Student's t test). The improved thermoregulation of wild type mice during a second swim at 26°C correlated with their greater immobility whereas defense against the warmth during a swim at 41°C correlated better with greater immobility of UCP2-deficient mice. Together these data indicate that while the lack of UCP2 has no acute effect on body temperature, UCP2 may inhibit rapid improvements in defense against cold, in contrast to UCP1, whose main function is to promote thermogenesis.

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“…The elevation in basal body temperature appears to be mediated by stress induced changes to the thermoregulatory response of the mPOA (Long et al, 1990; Briese & Cabanac, 1991; Hayashida et al, 2010), but the mechanisms underlying these changes are unknown. The mPOA has warm-sensitive neurons to keep heat-production and heat-loss in equilibrium to maintain homeostatic body temperature under normal ambient conditions.…”

Section: Discussionmentioning

confidence: 99%

“…Repeated exposures to unpredictable stressors can dysregulate normal stress responses to cause pathological alterations in mood, cognition and physiological function (McEwen, 2003). One such physiological function affected by stress is thermoregulation where chronic stress exposure causes sustained elevation in body temperature up to 60 days after termination of stress (Timmerman et al, 1992; Endo & Shiraki, 2000; Oka et al, 2001; Matuszewich & Yamamoto, 2003; Hayashida et al, 2010). This long-lasting elevation in body temperature is attributed to a shift in brain set-point temperature, but the mechanism underlying this long-term shift in set-point is unknown (Kluger et al, 1987; Briese & Cabanac, 1991).…”

Section: Introductionmentioning

confidence: 99%

Protracted effects of chronic stress on serotonin-dependent thermoregulation

Natarajan

Northrop

Yamamoto

2015

Stress

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Chronic stress is known to affect serotonin (5HT) neurotransmission in the brain and to alter body temperature. Body temperature is controlled in part, by the medial preoptic area of the hypothalamus (mPOA). To investigate the effect of chronic stress on 5HT and how it affects body temperature regulation, we examined whether exposure to a chronic unpredictable stress paradigm (CUS) produces long-term alterations in thermoregulatory function of the mPOA through decreased 5HT neurotransmission. Adult male Sprague-Dawley rats underwent 21 days of CUS. Four days after last stress exposure, basal body temperature in the home cage and body temperature in a cold room maintained at 10°C were recorded. CUS rats had significantly higher subcutaneous basal body temperature at 13:00 h compared to unstressed (NoStress) rats. Whereas the NoStress rats were able to significantly elevate body temperature from basal levels at 30 and 60 min of exposure to the cold room, the CUS rats showed a hypothermic response to the cold. Treatment during CUS with metyrapone, a corticosterone synthesis inhibitor, blocked stress-induced decrease in body temperature in response to the cold challenge. CUS also decreased 5HT transporter protein immunoreactivity in the mPOA and 5HT2A/C agonist injection into the mPOA after CUS exposure caused stressed rats to exhibit a sensitized hyperthermic response to cold. These results indicate that CUS induced changes to the 5HTergic system alters mPOA function in thermoregulation. These findings help explain mechanisms underlying chronic stress induced disorders such as chronic fatigue syndrome wherein long lasting thermoregulatory deficits are observed.

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Repeated social defeat stress induces chronic hyperthermia in rats

Cited by 49 publications

References 40 publications

Simultaneous Changes in Sleep, qEEG, Physiology, Behaviour and Neurochemistry in Rats Exposed to Repeated Social Defeat Stress

Simultaneous Changes in Sleep, qEEG, Physiology, Behaviour and Neurochemistry in Rats Exposed to Repeated Social Defeat Stress

After a cold conditioning swim, UCP2-deficient mice are more able to defend against the cold than wild type mice

Protracted effects of chronic stress on serotonin-dependent thermoregulation

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