Impulsivity and stress are two of the most important determinants of drug addiction in that both factors predict the initiation and maintenance of drug use, as well as relapse to drug taking following abstinence. Despite this combined influence, the interaction between stress and impulsivity has never been examined systematically in animal models of addiction. The objective of the current study is to examine the role of acute stress on two different measures of impulsivity in rats: the Go/No-go test measures motor impulsivity, and the Delayed Reinforcement Paradigm measures cognitive impulsivity. To determine whether a 1 hr restraint stress is physiologically stressful, blood samples from rats in Experiment 1 were taken at 5 different sampling points: baseline (0 min), reactivity (15 and 60 min) and recovery (100 and 180 min). In Experiments 2 and 3, rats were tested in either the Go/No-go test or the Delayed Reinforcement test immediately following 1 hr of restraint stress. Results from Experiment 1 show that 1 hr of restraint stress increased plasma corticosterone concentrations at 15 min and 60 min; corticosterone concentrations returned to baseline levels by 100 min. Following stress, the percentage of Go interval responding was not altered during Go/No-go testing (Experiment 2), nor were there changes in the indifference point values during Delayed Reinforcement testing (Experiment 3). These results suggest that 1 hr of acute stress does not increase either motor or cognitive impulsivity, and stress may influence addiction via mechanisms that are independent of impulsivity. / Thesis (Master, Psychology) -- Queen's University, 2009-08-24 15:17:00.597

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Indiana University-Purdue University Indianapolis (IUPUI) / The opioid crisis has resulted in an unprecedented number of neonates born with prenatal opioid exposure; however, the long-term effects of opioid exposure on offspring behavior and neurodevelopment remain relatively unknown. I developed a translational mouse model of prenatal methadone exposure (PME) that resembles the typical pattern of opioid use by pregnant women who first use oxycodone then switch to methadone maintenance pharmacotherapy, and subsequently become pregnant while maintained on methadone. PME produced substantial impairments in offspring growth, sensorimotor milestone acquisition, and activity in an open field. Furthermore, these behavioral alterations were associated with significant disruptions in the primary motor cortex (M1). Notably, layer 5 pyramidal neurons of the M1 displayed significantly increased voltage sag which is primarily mediated by HCN1 channels. Interestingly, the α2-adrenergic receptor, a known modulator of HCN1 channels, displayed significantly increased expression in the M1 of PME animals. The locomotor activity in an open field was significantly reduced following in vivo pharmacological activation of the α2-adrenergic receptor with clonidine in PME offspring suggesting this may be therapeutic target for the hyperactivity associated with prenatal exposure to opioids. Previous work has also described an association between prenatal opioid exposure and alterations in opioid reward-related behavior; however, the effect of PME on alcohol reward remains undetermined. Given the widespread accessibility and usage, alcohol represents the most likely addictive substance the growing population of opioid exposed neonates will encounter as they age. I discovered that PME disrupts conditioned preference for alcohol, enhances the locomotor stimulating effects of alcohol, and increases alcohol consumption in a sex-dependent manner. This alcohol-reward phenotype in PME offspring was associated with altered excitatory neurotransmission and disrupted cannabinoid-mediated long-term depression (CB-LTD) in the dorsolateral striatum, an important substrate involved in compulsive drug use. Further work is required to determine the specific inputs at which CB-LTD is disrupted and if restoring this form of plasticity in PME animals prevents the enhanced alcohol addiction phenotype. / 2023-03-02

Thesis (Ph. D.)--University of Washington, 1997. / Vita. Includes bibliographical references (leaves [59-68).

Thesis (Ph. D.)--West Virginia University, 2009. / Title from document title page. Document formatted into pages; contains vi, 95 p. Includes abstract. Includes bibliographical references (p. 56-64).

Thesis (Ph. D.)--University of Rhode Island, 2004. / Typescript. Includes bibliographical references (leaves 89-97).

Thesis (J.C.L.)--Catholic University of America, 2003. / Includes bibliographical references (leaves 47-52).

Thesis (J.C.L.)--Catholic University of America, 2003. / Includes bibliographical references (leaves 47-52).

Thesis (Ph.D.)--York University, 2008. Graduate Programme in Communication and Culture. / Typescript. Includes bibliographical references (leaves 261-277). Also available on the Internet. MODE OF ACCESS via web browser by entering the following URL: http://gateway.proquest.com/openurl?url_ver=Z39.88-2004&res_dat=xri:pqdiss&rft_val_fmt=info:ofi/fmt:kev:mtx:dissertation&rft_dat=xri:pqdiss:NR51780

Thesis (M.A.)--Rowan University, 2006. / Typescript. Includes bibliographical references.