Emotional Memory Modulation

Abstract

Emotionally arousing and stressful experiences are often remembered better than neutral ones. Stress hormones, including norepinephrine and glucocorticoids, are traditionally thought to enhance memory consolidation, but accumulating evidence suggests that they also shape memory specificity and generalization. This is particularly relevant to stress-related psychopathologies such as post-traumatic stress disorder (PTSD), where fear overgeneralization and impaired safety learning may contribute to persistent symptoms. Moreover, individuals differ substantially in their physiological stress responses, potentially influencing how emotional memories are processed. In this thesis, I examined in rats how norepinephrine and glucocorticoids modulate memory specificity and generalization, the underlying neural circuitry, and how endogenous differences in stress hormone signaling influence these processes. Across experiments, norepinephrine and glucocorticoids exerted opposing effects: noradrenergic activation promoted memory specificity, whereas glucocorticoid signaling promoted generalization, particularly when discrimination between experiences was required. Furthermore, individual differences in HPA-axis regulation influenced the response to glucocorticoid treatment. These findings demonstrate that stress hormones do not simply enhance memory, but differentially bias memory toward specificity or generalization. They further demonstrate that individual differences can affect responses to pharmacological treatment, highlighting the importance of personalized approaches to PTSD treatment.