Physical versus psychological social stress in male rats reveals distinct cardiovascular, inflammatory and behavioral consequences

Abstract

Repeated exposure to social stress can precipitate the development of psychosocial disorders including depression and comorbid cardiovascular disease. While a major component of social stress often encompasses physical interactions, purely psychological stressors (i.e. witnessing a traumatic event) also fall under the scope of social stress. The current study determined whether the acute stress response and susceptibility to stress-related consequences differed based on whether the stressor consisted of physical versus purely psychological social stress. Using a modified resident-intruder paradigm, male rats were either directly exposed to repeated social defeat stress (intruder) or witnessed a male rat being defeated. Cardiovascular parameters, behavioral anhedonia, and inflammatory cytokines in plasma and the stress-sensitive locus coeruleus were compared between intruder, witness, and control rats. Surprisingly intruders and witnesses exhibited nearly identical increases in mean arterial pressure and heart rate during acute and repeated stress exposures, yet only intruders exhibited stress-induced arrhythmias. Furthermore, re-exposure to the stress environment in the absence of the resident produced robust pressor and tachycardic responses in both stress conditions indicating the robust and enduring nature of social stress. In contrast, the long-term consequences of these stressors were distinct. Intruders were characterized by enhanced inflammatory sensitivity in plasma, while witnesses were characterized by the emergence of depressive-like anhedonia, transient increases in systolic blood pressure and plasma levels of tissue inhibitor of metalloproteinase. The current study highlights that while the acute cardiovascular responses to stress were identical between intruders and witnesses, these stressors produced distinct differences in the enduring consequences to stress, suggesting that witness stress may be more likely to produce long-term cardiovascular dysfunction and comorbid behavioral anhedonia while exposure to physical stressors may bias the system towards sensitivity to inflammatory disorders.

Maternal social environment affects offspring cognition through behavioural and immune pathways in rats

“…CSS, in comparison with SE, affected maternal immune factors, increasing TIMP‐1 and ICAM‐1, and slightly impaired offspring cognition. Our results support previous studies reporting increased plasma TIMP‐1 following social stress in the rat and up‐regulated TIMP‐1 mRNA expression in the prefrontal cortex of mice exposed to CSS . Elevated glucocorticoids can inhibit ICAM‐1 expression .…”

Inflaming sex differences in mood disorders

“…Male mice had significantly elevated levels of IL-6 after witnessing social defeat [213]. A number of inflammatory cardiac factors were altered following social defeat stress [218,219], and were replicated in vicarious social defeat stress [220]. As this model is now being used in females [215], it will be very interesting to examine cytokine profiles and determine whether the same peripheral indicators of stress are activated in both sexes.…”

A novel construct of anhedonia revealed in a Chinese sample via the Revised Physical and Social Anhedonia Scales

“…There is a long history and broad acceptance of viewing mental disorders in relation to physical sensation and social function, and this perspective is well represented in diagnostic criteria. These bases are also amenable to experimental exploration of the nature of anhedonia in animal experiments [68,69]. The more recent temporal components of anhedonia, namely anticipatory anhedonia and consummatory anhedonia [7], were also supported by our hierarchy analysis of the concept of anhedonia.…”