Chronic social stress in mice causes behavioral and physiological changes resulting in perturbed rhythms of body temperature, activity and sleep-wake cycle. To further understand the link between mood disorders and temperature rhythmicity, we measured core body temperature (Tcore) in mice before and after exposure to the chronic social defeat stress (CSDS) paradigm. Our results revealed that Tcore amplitudes of stress resilient and susceptible mice are dampened during exposure to CSDS. However, after exposure to social stress, the temperature amplitude of resilient mice recovered faster than the susceptible mice. There were minimal changes in locomotor activity after stress exposure which correlates with regular rhythmic expression of Prok2, an output signal of the SCN (Suprachiasmatic nucleus). We also investigated the molecular changes associated with these dampened temperature rhythms, and determined the expression levels of thermosensitive genes Cirbp, Rbm3 and Hsf1. Expression of Rbm3 and Cirbp in the LHb (Lateral habenula) were blunted 1 day after CSDS. These molecular rhythms recovered 10 days later such that daytime expression was higher compared to nighttime, similar to stress-naive controls. Hsf1 did not show robust rhythmic expression in the LHb.
Chronic social stress in mice causes behavioural and physiological changes that result in perturbed rhythms of body temperature, activity and sleep-wake cycle. To further understand the link between mood disorders and temperature rhythmicity in mice that are resilient or susceptible to stress, we measured core body temperature (Tcore) before and after exposure to chronic social defeat stress (CSDS). We found that Tcore amplitudes of stress-resilient and susceptible mice are dampened during exposure to CSDS. However, following CSDS, resilient mice recovered temperature amplitude faster than susceptible mice. Furthermore, the interdaily stability (IS) of temperature rhythms was fragmented in stress-exposed mice during CSDS, which recovered to control levels following stress. There were minimal changes in locomotor activity after stress exposure which correlates with regular rhythmic expression of
Prok2
- an output signal of the suprachiasmatic nucleus. We also determined that expression of thermosensitive genes
Rbm3
and
Cirbp
in the lateral habenula (LHb) were blunted 1 day after CSDS. Rhythmic expression of these genes recovered 10 days later. Overall, we show that CSDS blunts Tcore and thermosensitive gene rhythms. Tcore rhythm recovery is faster in stress-resilient mice, but
Rbm3
and
Cirbp
recovery is uniform across the phenotypes.
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