Date of Award

5-2026

Degree Type

Thesis

Degree Name

Master of Science

Department

Biology

Program

Integrated Biosciences (MS)

First Advisor/Chairperson

Amber LaCrosse

Abstract

Post-traumatic stress disorder (PTSD) is a chronic psychiatric disorder and the most common disorder following exposure to a traumatic event. The most commonly used drugs in PTSD treatment are selective serotonin reuptake inhibitors (SSRIs), though only about 50% of patients respond to this treatment. Previous work in our lab demonstrated the combination of chronic fluoxetine (FLX) and acute ketamine treatment decreased fear response in a contextual fear paradigm in male C57/BL mice. In rodents, fear conditioning (FC) is commonly used in the literature to induce behaviors related to PTSD. The mammalian central fear memory circuit involves a dynamic interplay between excitatory and inhibitory projections between the prefrontal cortex, hippocampus, and amygdala., Fear related disorders can be characterized by aberrations in GABAergic metabolism, with numerous studies demonstrating altered levels of GABA, its receptors, and glutamic acid decarboxylase (GAD65/67); its rate limiting enzyme. GABAergic interneurons function as essential regulators of fear memory through their direct inhibitory influence on excitatory pyramidal cells (PCs) throughout the amygdala, hippocampus, and PFC. This study quantified the expression GAD67/65 in brains harvested from mice that underwent FC and drug treatment from a previous published study conducted in our laboratory. Specifically, this research aims to assess the expression and function of inhibitory neuronal populations in the infralimbic prefrontal cortex (IL-PFC) and the CA1 region of the hippocampus. No overall group differences were observed across all five treatment groups in the ILPFC and CA1.

Access Type

Open Access

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Alex Ottimer.pdf (35 kB)
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