Abstract
Free-living animals encounter a wide range of ecological and environmental stressors throughout their lifetime, which can shape both cognitive performance and neural function. While cognitive abilities, particularly learning and memory, are critical for responding effectively to these stressors, evidence suggests that stress exposure – in particular glucocorticoid hormones – can, in turn, affect cognition. However, the neurobiological mechanisms underlying these bidirectional interactions remain poorly understood, especially in wild systems. Thus, in this dissertation, I investigated how chronic predation risk and glucocorticoid hormones influence cognition in wild white-footed mice (Peromyscus leucopus). I further examined the effects of predation risk on the relationship between neuronal activation patterns and cognitive performance. In Chapter 2, I show that chronic predation risk did not impair learning but had a small effect on memory, and affected exploratory behaviour, suggesting that exploration strategies might help animals maintain learning performance under chronic predation risk conditions. In Chapter 3, I show that glucocorticoids had no effect on associative learning and memory, but did affect spatial learning and memory, and the opposite pattern was true for long-term memory. Finally, in Chapter 4, I show how predation risk reduced neuronal activation patterns in the hippocampus and alters the relationship between neuronal activation patterns and cognitive performance. Overall, this work provides novel insight into how predation risk and stress hormones shape cognition and brain function in wild animals. These findings highlight the importance of studying neurobiological mechanisms in ecologically relevant contexts to better understand how animals maintain adaptive function under chronic environmental stress.