Date of Award:

5-2024

Document Type:

Dissertation

Degree Name:

Doctor of Philosophy (PhD)

Department:

Psychology

Committee Chair(s)

Mona Buhusi

Committee

Mona Buhusi

Committee

Brett Adams

Committee

Catalin Buhusi

Committee

Erin Bobeck

Committee

JoAnn Tschanz

Abstract

Major depressive disorder, or depression, is among the leading causes of disability globally. Despite being a large public health challenge, depression remains difficult to treat as the underlying biology is still unknown and the currently available treatments are limited in effectiveness. This experiment was to test the efficacy of the drug LM11A-31, which works on the signaling pathway of proneurotrophin-p75NTR, a pathway that is not targeted by any currently used antidepressants. Male mice underwent a repeated forced swim, with all the mice receiving saline the first two days and then half the mice receiving saline and half receiving LM11A-31 before the swim on the last day. Increased immobility in the swim was recorded as a measure of depression or "behavioral despair." A second experiment was conducted to determine if LM11A-31 increased overall activity or anxiety, which could be confound factors for the forced swim results. The outcome of both experiments points to LM11A-31 having antidepressant properties. This is significant as it suggests that proneurotrophin-p75NTR signaling may underlie symptoms of depression, gives a new drug that has antidepressant potential that works in a different way than any currently used antidepressants, and validates proneurotrophin-p75NTR as a novel target for future antidepressant drug development.

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