Theses and Dissertations
This collection includes both ASU Theses and Dissertations, submitted by graduate students, and the Barrett, Honors College theses submitted by undergraduate students.
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Description
Fibromyalgia (FM) is a chronic musculoskeletal disorder characterized by widespread pain, fatigue, and a variety of other comorbid physiological and psychological characteristics, including a deficit of positive affect. Recently, the focus of research on the pathophysiology of FM has considered the role of a number of genomic variants. In the current manuscript, case-control analyses did not support the hypothesis that FM patients would differ from other chronic pain groups in catechol-O-methyltransferase (COMT) and mu-opioid receptor (OPRM1) genotype. However, evidence is provided in support of the hypothesis that functional single nucleotide polymorphisms on the COMT and OPRM1 genes would be associated with risk and resilience, respectively, in a dual processing model of pain-related positive affective regulation in FM. Forty-six female patients with a physician-confirmed diagnosis of FM completed an electronic diary that included once-daily assessments of positive affect and soft tissue pain. Multilevel modeling yielded a significant gene X environment interaction, such that individuals with met/met genotype on COMT experienced a greater decline in positive affect as daily pain increased than did either val/met or val/val individuals. A gene X environment interaction for OPRM1 also emerged, indicating that individuals with at least one asp allele were more resilient to elevations in daily pain than those homozygous for the asn allele. In sum, the findings offer researchers ample reason to further investigate the contribution of the catecholamine and opioid systems, and their associated genomic variants, to the still poorly understood experience of FM.
ContributorsFinan, Patrick Hamilton (Author) / Zautra, Alex (Thesis advisor) / Davis, Mary (Committee member) / Lemery-Chalfant, Kathryn (Committee member) / Presson, Clark (Committee member) / Arizona State University (Publisher)
Created2011
Description
Opioid use rates and related deaths continue to be a public health crisis; while there are many contributing factors to opioid use disorders, criteria for diagnosis include problems related to social functioning. Previous research indicates that laboratory rats, which are frequently used as animal models of addiction-related behaviors, are capable of prosocial behavior. The following collection of studies were performed to determine the effects of heroin on prosocial behavior in rats, as well as the role of the insula in both self-administration of heroin and prosocial behaviors. All of the experiments were conducted utilizing an established model of prosocial behavior in rats in which a performing rat releases a cagemate from a restrainer. The occurrence of and latency to free the confined rat was recorded. After baseline rescuing behavior was established, rats were allowed to self-administer heroin (0.06 mg/kg/infusion i.v.), and subsequent experimental conditions were imposed.
Experimental conditions, in a series of different studies, included comparing heroin reinforcers with sucrose, chemogenetically modulating the insular cortex (both stimulatory and inhibitory processes) and administering excitotoxic lesions in the insula. There were significant differences in saving behaviors between heroin and sucrose groups demonstrating an opioid induced loss of prosocial behavior. Modulating the insula chemogenetically resulted in some restoration of these opioid related deficits, and insular lesions did not significantly impact prosocial behaviors, however, there were significant differences between rates of heroin intake in lesioned animals versus non-lesioned controls. Taken together, these results demonstrate the deleterious effects of heroin on prosocial behaviors and offer further support for the role of the insula in both addiction and social constructs.
Experimental conditions, in a series of different studies, included comparing heroin reinforcers with sucrose, chemogenetically modulating the insular cortex (both stimulatory and inhibitory processes) and administering excitotoxic lesions in the insula. There were significant differences in saving behaviors between heroin and sucrose groups demonstrating an opioid induced loss of prosocial behavior. Modulating the insula chemogenetically resulted in some restoration of these opioid related deficits, and insular lesions did not significantly impact prosocial behaviors, however, there were significant differences between rates of heroin intake in lesioned animals versus non-lesioned controls. Taken together, these results demonstrate the deleterious effects of heroin on prosocial behaviors and offer further support for the role of the insula in both addiction and social constructs.
ContributorsTomek, Seven Eli (Author) / Olive, Michael F (Thesis advisor) / Neisewander, Janet (Committee member) / Wynne, Clive (Committee member) / Comer, Sandra (Committee member) / Arizona State University (Publisher)
Created2020