Document Type

Honors Project

Publication Date

6-10-2026

Abstract

Postpartum depression is a heterogeneous psychological disorder affecting nearly 20% of individuals who have given birth. Widely prescribed serotonin reuptake inhibitors (SSRIs) can transfer into breastmilk, which may impact offspring neuronal activity and neurodevelopment. Maternal SSRI use has been associated with hyperserotonemia, a condition of elevated blood serotonin levels, which is observed in more than 25% of individuals diagnosed with autism spectrum disorder- a neurodevelopmental condition characterized by altered social behavior and differences in brain stimulus recognition patterns. Disrupted oxytocin signaling has been reported in individuals with hyperserotonemia and reduced neuronal activity within this circuit has also been observed following SSRI exposure in mice. Oxytocin is synthesized by magnocellular neurons in the paraventricular nucleus of the hypothalamus (PVN) and their axons project to the medial amygdala (MeA). Both regions play key roles in social recognition and bonding. Using a mouse model, we will examine how developmental fluoxetine exposure, a SSRI, affects neural circuits underlying social behavior across sex by quantifying c-Fos as a marker of neuronal activity and oxytocinergic cell activation in the PVN and in the MeA following interaction with a novel social stimulus. This thesis focuses on the optimization of the oxytocin and c-Fos double-label immunofluorescence protocol, which has been developed and refined over two years, and contributes to the overall project. Ultimately, this research seeks to empirically determine how postnatal antidepressant exposure influences offspring neurodevelopment, with the intention of generating evidence to better support maternal decision- making and long-term offspring health.

Level of Honors

magna cum laude

Department

Biology

Department

Neuroscience

Advisor

Elizabeth DeStasio

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Available for download on Tuesday, June 10, 2031

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