Characterizing the long-lasting impact of stress in mid-adolescence in the rat.
Exposure to stressors in adolescence, in both humans and rodents, leads to long-lasting alterations in their behaviour and corresponding neuroanatomical structures. The experiments presented herein were designed to further investigate the lasting impact of intermittent physical stress (elevated platform, foot shock, water immersion) in mid-adolescence on adult behaviour and neuroanatomy. Previously, I demonstrated that exposure to this intermittent physical stress protocol led to differential outcomes if the stressors were experienced during different periods within adolescence (i.e., early vs. mid-adolescence). The most intriguing outcome from that work was that exposure to intermittent physical stress in mid-adolescence (PD35-46) led to paradoxical increases in exploration of typically avoided areas of the Elevated Plus Maze. In Chapter 2 of this dissertation, I now demonstrate that this increase in exploration is modified based on the amount of social contact rats experience across adolescence whereby increasing the amount of social contact during adolescence normalized the increases in exploration. This suggests that affiliative social contact buffers the lasting impact of stress in mid-adolescence and might, in some instances, promote resilience to subsequent stressors in later life. In Chapter 3, I demonstrate that exposure to intermittent physical stress in mid-adolescence not only increases rats’ exploration of open areas of the plus-maze, it also increases their sensitivity to the locomotor enhancing effects of amphetamine, such that their levels of exploration predicted their locomotor response. Further analysis supported the idea that experiencing intermittent physical stress in mid-adolescence promotes a shift in rats’ behavioural response from a security-centric toward a more reward-centric phenotype. In Chapter 4, I argue that this shift might be due, at least in part, to the stress-induced dendritic remodeling of pyramidal neurons in the anterior basolateral amygdala. Collectively, these findings suggest that exposure to stressors, when restricted to mid-adolescence, promotes neuroanatomical and behavioural changes that facilitate risk-taking phenotypes.