Social buffering of the stress response: insights from fishes.

Social buffering of stress refers to the effect of a social partner in reducing the cortisol or corticosterone response to a stressor. It has been well studied in mammals, particularly those that form pair bonds. Recent studies on fishes suggest that social buffering of stress also occurs in solitary species, gregarious species that form loose aggregations and species with well-defined social structures and bonds. The diversity of social contexts in which stress buffering has been observed in fishes holds promise to shed light on the evolution of this phenomenon among vertebrates. Equally, the relative simplicity of the fish brain is advantageous for identifying the neural mechanisms responsible for social buffering. In particular, fishes have a relatively small and simple forebrain but the brain regions that are key to social buffering, including the social behaviour network, the amygdala and the hypothalamic-pituitary-adrenal/interrenal axis, are functionally conserved across vertebrates. Thus, we suggest that insight into the mechanistic and evolutionary underpinnings of stress buffering in vertebrates can be gained from the study of social buffering of stress in fishes.

Elevated cortisol lowers thermal tolerance but results in limited cardiac remodelling in rainbow trout (Oncorhynchus mykiss) experiencing chronic social stress.

Juvenile rainbow trout (Oncorhynchus mykiss) held in pairs form dominance hierarchies in which subordinate individuals experience chronic social stress accompanied by lowered thermal tolerance (assessed as the critical thermal maximum, CTmax). Here, we tested the hypothesis that chronic elevation of circulating cortisol levels reduces thermal tolerance in subordinate trout. In support of this hypothesis, subordinate trout that recovered from social stress for 48 h, a period sufficient to return cortisol to normal baseline levels, no longer showed reduced CTmax. Further, thermal tolerance was not restored in subordinates treated with cortisol during recovery from social stress. To explore possible mechanisms underlying the effect of chronic stress on CTmax, we also tested the hypothesis that chronic cortisol elevation induces cardiac remodelling in subordinate trout, as previously reported for cortisol-treated rainbow trout. Ventricle mass and cardiac hypertrophy markers were unaffected by social stress. Picrosirius Red staining revealed a trend for lower collagen levels in the ventricles of subordinate relative to dominant trout. However, collagen type I transcript and protein levels, and markers of collagen turnover were unaffected. Indicators of cardiac function, including ventricle passive stiffness and intrinsic heart rate (fH), similarly were unaffected. In vivo fH was also similar between subordinate and dominant fish. Nevertheless, in keeping with their lower CTmax, subordinate fish exhibited cardiac arrhythmia at significantly lower temperatures than dominant fish during CTmax trials. Thus, high baseline cortisol levels in subordinate trout result in lowered thermal tolerance, but 5 days of social stress did not greatly affect cardiac structure or function.