Abstract
Psychosocial stressors (e.g., anxiety, personality traits, social isolation) are risk factors for cardiovascular events and heart disease. However, there is a lack of knowledge regarding the biological mechanisms that underlie this risk-outcome relationship. To address this knowledge gap, our team uses two non-traditional animal models, the Syrian hamster ( Mesocricetus auratus ) and gray short-tailed opossum ( Monodelphis domestica ). We previously reported that social isolation-induced aggression, a type of psychosocial stress experience, leads to increased neural activation in the ventral tegmental area (VTA) of the midbrain. The VTA contains tyrosine hydroxylase (TH)-producing (putative dopamine, DA) neurons and is innervated by vasopressin (AVP) fibers. DA and AVP play a role in social behavior, and we investigated whether these two systems interact when an individual experiences psychosocial stress-induced aggression. Here we report that social interactions increased Fos, the protein product of the immediate early gene c-fos that serves as a marker of neuronal activation, in non-TH cells in an area of the VTA called the interfascicular nucleus (IF) of male subjects. Previous social experience increased the number of TH-positive cells in the IF but had no effect on the number of AVP-ir fibers. Conversely, levels of aggressive and social dominance behaviors were positively correlated with the number of AVP-ir fibers in the IF, whereas there was no relationship between these behaviors and the number of TH-positive cells. In socially naïve males, AVP microinjected into the VTA inhibited the duration of aggressive behavior. We are currently investigating the impact of our psychosocial stress paradigms on myocardial injury in both males and females. Our results suggest a complex interaction between AVP and DA systems in the brain in psychosocial stress responses. Our long-term goal is to build on these preliminary findings to determine whether AVP in the VTA may reduce psychosocial stress-induced myocardial injury, a first step in exploring heart-brain interactions that may link psychosocial stress with negative cardiovascular disease outcomes.
Published Version
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