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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- Creators: School of Life Sciences
Description
Incentive salience is a motivational-cognitive process that can transform an otherwise neutral stimulus into something that is wanted. The prolonged use of nicotine appears to enhance incentive salience; it has been suggested that the nicotinic enhancement of incentive salience contributes to the potential of relapse in individuals with tobacco addiction. In order to determine whether (a) nicotinic enhancement of incentive salience for non-nicotinic stimuli occurs when rats self-administer nicotine and (b) a history of nicotine use facilitates such enhancement, rats were trained in a morning self-administration paradigm (SA), in combination with an afternoon 4-CS Pavlovian conditioned approach task (PCA) for 24 days. SA was followed by extinction and cue reinstatement. Nicotine SA enhanced incentive salience in the PCA. Upon extinction, incentive salience quickly declined to saline levels, indicating that the nicotinic enhancement of incentive salience is transient. Experimenter-administered nicotine enhanced incentive salience similarly regardless of nicotine history, suggesting that a previous history of nicotine use does sensitize the nicotinic enhancement of incentive salience. Taken together, these results suggest that nicotine must be onboard for the expression of nicotinic enhancement of incentive salience. This suggests that the role of incentive salience in the development and relapse of tobacco addiction may need to be revisited.
ContributorsOverby, Paula F. (Author) / Sanabria, Federico (Thesis director) / Gipson-Reichardt, Cassandra (Committee member) / Beckmann, Joshua (Committee member) / School of Life Sciences (Contributor) / Department of Psychology (Contributor) / Barrett, The Honors College (Contributor)
Created2017-05
Description
Aberrant signaling through the canonical RAS/RAF/MEK/ERK (ERK/MAPK) pathway leads to the pathology of a group of neurodevelopmental disorders called RASopathies. RASopathies are caused by germline mutations in the ERK/MAPK pathway and have an incidence of approximately 1:2000 births. The majority of RASopathies stem from mutations that cause gain-of-function in the ERK/MAPK pathway. In this study, we have begun to unravel the roles that GABAergic interneurons play in the pathology of RASopathies. Our data demonstrate that gain-of-function ERK/MAPK signaling expressed in a GABAergic interneuron-specific fashion leads to forebrain hyperexcitability in mutant mice. Further, some GABAergic interneurons experience activated-caspase 3 mediated apoptosis in the embryonic subpallium, leading to a loss of PV-expressing interneurons in the somatosensory cortex. We found that pharmaceutical intervention during embryogenesis using a MEK1 inhibitor may be effective in preventing apoptosis of these neurons. Future work is still needed to understand the mechanism of the death of GABAergic interneurons and to further pursue therapeutic approaches. Taken together, this study suggests potential roles of cortical GABAergic interneurons in ERK/MAPK-linked pathologies and indicates possible approaches to provide therapy for these conditions.
ContributorsShah, Shiv (Author) / Newbern, Jason (Thesis director) / Gipson-Reichardt, Cassandra (Committee member) / School of Life Sciences (Contributor) / Economics Program in CLAS (Contributor) / Barrett, The Honors College (Contributor)
Created2019-05
Description
Adolescent mental health problems are predicative of future problems such as depression, anxiety, ADHD, compulsive disorder, and substance use. Previous studies show that in emerging adulthood, the high prevalence and associated burdens of psychopathology increase vulnerability to disorders. These diagnoses are less common but are more severe and chronic (Tanner et al., 2009). The causes of these disorders are still being explored with recent studies showing that these mental health problems are genetically influenced. This makes understanding which gene that corresponds to what biological system is important in determining mental health. From recent studies, genes that code for calcium channels are good candidates for mental health problems. These voltage-gated channels are important mediators for physiological functions in the central nervous system and their activation provides unique responses within the brain. In a previous study, it supports the association of polymorphisms in calcium and potassium channels with the genetic risk for bipolar disorders and other mental illness (Imbrici et al., 2013). The purpose of the study was to examine if calcium channel genes influence childhood psychiatric symptoms. The first goal of this study was to form a polygenic risk score representing genetic influence on calcium channels. The second goal was to use this risk score in genetic association analyses to understand genetic risk for childhood psychopathology. Overall, the study did accomplish the goal as a polygenic risk score was created and was used to examine genetic association with child psychopathology. Based on the results, the polygenic risk score was not correlated with either parent or child- reported symptoms; however, results did show that disorders were related to each other and differed by race.
ContributorsTang, Derek (Author) / Lemery, Kathryn (Thesis director) / Gipson-Reichardt, Cassandra (Committee member) / Elam, Kit (Committee member) / School of Life Sciences (Contributor) / Barrett, The Honors College (Contributor)
Created2018-05
Description
The present study examined how systemic low doses of nicotine affect the microstructure of food-reinforced behavior in rats. Rats were given an acute saline or nicotine treatment (0.1-0.6 mg/kg, resting at least 48 h between injections), and a chronic saline or nicotine treatment (0.3 mg/kg for 10 consecutive days). Immediately after treatment, rats were required to press a lever to obtain food, whose availability was unpredictable, but programmed at a constant rate (on average every 80 s). Acute nicotine dose-dependently suppressed behavior prior to the delivery of the first reinforcer, but enhanced food-reinforced behavior afterwards. This effect was primarily observed in the time it took rats to initiate food-seeking behavior, and not in the food-seeking behavior itself. A pre-feeding control procedure suggests that these effects cannot be explained only by changes in appetite. Over the course of chronic nicotine exposure, tolerance developed to the suppressive, but not to the enhancing effects of nicotine on food-seeking behavior. These results suggest that ostensive sensitization effects of nicotine on behavior may instead reflect a tolerance for its suppressive effects on behavior.
ContributorsRomero, Korinna Estela (Author) / Sanabria, Federico (Thesis director) / Gipson-Reichardt, Cassandra (Committee member) / Bevins, Rick (Committee member) / Department of Psychology (Contributor) / School of Life Sciences (Contributor) / Barrett, The Honors College (Contributor)
Created2017-05