عواقب رفتاری دو پارادایم استرس روانی- اجتماعی مزمن: اضطراب بدون افسردگی

Chronic stress, in particular chronic psychosocial stress, is a risk factor in the aetiology of various psychopathologies including anxiety- and depression-related disorders. Therefore, recent studies have focussed on the development of social-stress paradigms, which are believed to be more relevant to the human situation than non-social-stress paradigms. The majority of these paradigms have been reported to increase both anxiety- and depression-related behaviour in rats or mice. However, in order to dissect the mechanisms underlying anxiety or depression, animal models are needed, which specifically induce one, or the other, phenotype. Here, we study both short- (1 d after stressor termination) and long-term (4 d or 7 d after stressor termination) behavioural and physiological consequences of two well-validated chronic psychosocial stress models: social-defeat/overcrowding (SD/OC) and chronic subordinate colony housing (CSC). We demonstrate that SD/OC and CSC result in different physiological alterations: SD/OC more strongly affecting body-weight development, whereas CSC more strongly affects adrenal and pituitary morphology. Both stressors were shown to flatten circadian locomotor activity immediately after stress termination, which normalized 7 d later in SD/OC group but reversed to hyperactivity during the dark phase in the CSC group. Importantly, neither stress paradigm resulted in an increase in depression-related behaviour as assessed using the forced swim test, tail suspension test and saccharin preference test at any time-point. However, both stress paradigms lead to an anxiogenic phenotype; albeit with different temporal profiles and not towards a novel con-specific (social anxiety). CSC exposure elevates anxiety-related behaviour immediately after stressor termination, which lasts for at least 1 wk. In contrast, the anxiogenic phenotype only develops 1 wk after SD/OC termination. In conclusion, both models are unique for uncovering the molecular underpinnings of anxiety-related behaviour without conflicting depression-based alterations.