Date of Award

Spring 2023

Document Type



Biological Science


College of Natural and Health Sciences

Primary Advisor

Dr. Todd Schraw


PTSD affects about 5% of adults in the United States every year.1 This thesis investigates the common biologic therapies for PTSD and the specificity factor of the catecholamine binding to related norepinephrine alpha-2A adrenergic receptors. The binding of these catecholamines to adrenaline receptors in the spinophilin cofilin axis of the dorsal hippocampus causes fear-memory modulation and storage by altering dendritic morphology and thus manipulating neuronal plasticity. Targeting the inhibition of these respective receptors and increasing the activity of cofilin, a protein responsible for breaking down actin utilized for dendrite reaction to stimulus appears promising. By preventing the binding of catecholamines in this axis which would depress cofilin, dendritic changes of elongation would be small rather than dramatized and prolonged as seen in PTSD, eliminating a change in plasticity and future responsiveness to recurring stimuli. The use of a polyclonal antibody rather than an SSRI or beta blocker – which only treats symptoms without changing the modulation of fear itself– was proposed due to the more bodily ‘holistic’ approach to PTSD rather than using an artificially synthesized pharmaceutical. Coupling the proposed antibody treatment with cognitive behavioral therapy can aid in making long term PTSD symptoms a thing of the past.