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    The impact of trait anxiety and psychosocial stress on sympathetic neural control in humans
    (Montana State University - Bozeman, College of Letters & Science, 2023) Bigalke, Jeremy Andrew; Chairperson, Graduate Committee: Cara A. Palmer; This is a manuscript style paper that includes co-authored chapters.
    Anxiety is highly prevalent, and while it is often adaptive, excessive stress and anxiety may predispose individuals to a heightened risk of cardiovascular disease. While excessive activity of the sympathetic nervous system (SNS) may underlie this association, direct measures of muscle sympathetic nerve activity (MSNA) indicate little, if any, alterations in resting sympathetic outflow in individuals with anxiety disorders. Assessment of the relationship between trait anxiety, MSNA, and blood pressure using a large cohort of healthy adults has not yet been conducted. Further, utilization of stress tasks within microneurographic settings that minimize the potential influence of breathing alterations, muscle movement, and other variables on the typically observed inter-individual variability in MSNA responsiveness to mental stress are needed to adequately assess the sole contribution of psychological stress on sympathetic neural activity. In Study 1, the association between trait anxiety, MSNA, and resting blood pressure was assessed in a population of 88 healthy adults, representing the largest study to date pairing trait anxiety with directly recorded sympathetic outflow to the periphery. Our findings indicate an independent relationship between trait anxiety, MSNA, and blood pressure when controlling for both age and sex. In Study 2, we utilized the trier social stress test (TSST) to assess the impact of anticipatory stress on MSNA and blood pressure in 28 healthy adults. Our findings showed that anticipatory stress is associated with increased blood pressure and reduced MSNA. Additionally, this appears to be baroreflex mediated as the magnitude of changes in blood pressure were directly proportional to reductions in MSNA, a relationship that was weakened or nonexistent during the active speech portion of the task. Lastly, anticipatory MSNA responsiveness accurately predicted reactivity to subsequent stress tasks. Together, these studies highlight a key relationship between both chronic, and acute psychological stress and anxiety on sympathoneural function in healthy adults.
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    Olfactory behavior as an indicator of prion infection
    (Montana State University - Bozeman, College of Letters & Science, 2011) Williams, Nikolas Scott; Chairperson, Graduate Committee: A. Michael Babcock
    The current project sought to identify changes in olfactory-related behavior in hamsters infected with the HY transmissible mink encephalopathy (HY TME) strain of the pathological form of the prion protein. Experiment 1 was conducted to validate an olfactory preference paradigm for use with Syrian golden hamsters. An experimental group was induced with anosmia by treating them with methimazole. In an olfactory preference test in which the time subjects spent investigating attractive, aversive, and neutral olfactory stimuli were assessed, control animals spent a significantly longer amount of time investigating the attractive versus aversive scents. The methimazole-treated group did not demonstrate this pattern. Experiment 2 investigated changes in olfactory behavior as a result of prion infection. A group of hamsters was infected with HY TME and subjected to olfactory preference testing at four time points: 20, 40, 60, and 80 days post inoculation. In addition, parallel subjects were sacrificed and submitted to immunohistochemical analysis in order to examine the proliferation of HY TME throughout olfactory-related brain structures with the intention of relating behavioral changes to the progression of prion infection. Results indicated that HY TME subjects lost their ability to perceive the attractive scent early in the disease. However, avoidance of the aversive scent was retained until much later. The immunohistochemistry revealed an initial appearance of the pathologic prion at 20 days post inoculation in the glomeruli of the olfactory bulb. Widespread infection throughout all olfactory structures was observed at 40 days post inoculation and beyond. These results suggested a differential sensory loss to the olfactory stimuli that may have been due to initial infection in the glomeruli and later infection in other olfactory structures. These findings support the utility of discrimination paradigms for the diagnosis of prion diseases.
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