Theses and Dissertations

Date of Award

2020

Document Type

Dissertation

Degree Name

Doctor of Philosophy (PhD)

Department

College of Psychology

First Advisor

Barry Nierenberg

Second Advisor

Ana Fins

Third Advisor

Travis Craddock

Fourth Advisor

Gordon Broderick

Keywords

clinical psychology, computational, depression, homeostatic, modeling, psychobiology

Abstract

The brain can be considered a complicated system of feedback mechanisms that maintain physiological homeostasis. Through psychological activity, neurochemicals act as homeostatic regulators. This study proposes that these components are part of a regulatory system that is capable of supporting multiple homeostatic regimes that, in turn, give rise to self-sustaining psychological behaviors. This project hypothesizes that such alternate regulatory programs may play a role in perpetuating psychological dysfunction. Interactions within and between components of the neurotransmitter network are represented as a set of discrete logic circuits. Neurotransmitter levels are linked to psychological constructs such as depression based on current literature. These networks were analyzed to find any stable regulatory regimes possible given the established connections. Analysis indicated that this model network supported two distinct and stable homeostatic regimes. The first corresponds to typical health, while the second presents with depression accompanied by increased and decreased levels of various neurochemicals. Treatment simulations were then run to mimic the effects of receiving an SSRI both in and out of the presence of stress, and to compare recidivism rates of returning to a normal regime to real-world statistics. This analysis suggests a new way to conceptualize depression as a naturally occurring stable regulatory regime within a complex neurotransmitter-psychobehavioral network system capable of supporting multiple stable states. Furthermore, it was found that efforts to shift the body’s stable regime from depression to health using SSRIs is impeded by stress, suggesting that some form of stress management would complement the effects of SSRI treatment.

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