Thesis title: Serotonin modulation of social behavior and neuroplasticity
To survive in a social environment, animals must evaluate threats from conspecifics and adjust their behavior accordingly. In mice, even a single episode of social defeat is sufficient to induce long-lasting changes, characterized by increased avoidance, immobility, and flight. These behavioral shifts are accompanied by specific engagement of serotonergic circuits. In this thesis, I investigated how serotonin contributes to the processing of acute social trauma. Using fiber photometry, I showed that serotonergic neurons in the median raphe and serotonin release in the ventral hippocampus are selectively activated during defeat, but not during neutral social interactions. To assess causality, I combined pharmacological depletion, chemogenetic inhibition, and optogenetic manipulations, revealing temporally distinct roles of serotonin during and after trauma in shaping defensive responses. Finally, I validated a new transgenic mouse line, the SNAP-GluR1, as a tool to study AMPA receptor dynamics in stress-related circuits, establishing its suitability for future applications. In conclusion, my PhD work demonstrates that serotonin critically regulates the immediate and delayed impact of social defeat on behavior, providing new insight into how neuromodulatory systems influence vulnerability and resilience to social stress.