Neural and endocrine mechanisms mediating prosociality

Prosociality, an inherent part of society, ensures the thriving and success of social groups. Understanding the role of stress on empathic prosocial behaviors, like helping behavior, is important for societal well-being, and for shedding light on stress-related neuropsychiatric diseases such as depression, social anxiety, and autism. As opposed to chronic and severe stressors, there is growing evidence linking acute/moderate levels of stress hormones to beneficial neural function and adaptive behaviors, and we propose a similar phenomenon might mediate helping behavior. We hypothesize that rats that have had their adrenal glands removed and therefore lack the phasic stress hormone responses (adrenalectomized rats) will demonstrate diminished helping behavior in a prosocial behavioral paradigm compared to rats that have undergone a sham procedure. Indeed, we find adrenalectomized rats display significantly less helping behavior compared to sham rats and that this effect is specific for the helping context, and not for normal social interactions, exploration, movement, or object interaction. Our preliminary immunohistochemical brain analyses find increased activation of the neural activity marker c-fos in the hippocampus of adrenalectomized rats compared to sham rats, which lends evidence for corticosterone, an adrenal stress hormone, having an effect on the hippocampus, which in turn has an effect on helping behavior. Since recent studies have implicated the hippocampus, and in particular the CA2 subregion, to be involved in social memory, our next step would be to directly reduce neural activity, either pharmacologically or optogenetically, in the hippocampus of adrenalectomized rats in hopes of restoring helping behavior. Our study helps illuminate how mechanistically, stress hormones modulate critical social circuits, and how this neural activity in turn affects complex behavioral outcomes.