Scholarship & Research

Now showing 1 - 3 of 3

Pupil response as a measure of preparatory control of attention in anticipation of deception
(Montana State University - Bozeman, College of Letters & Science, 2024) Brennan, Evan Michael; Chairperson, Graduate Committee: Keith A. Hutchison
Deception is generally considered to be more cognitively demanding than telling the truth, driving research interest in the relationship between deception and cognitive ability. Few studies have explored the preparatory attentional state occurring after the decision to be dishonest is made, but before the content of the question is known to the deceiver. Participants in the current study were given "Truth" or "Lie" prompts several seconds before being asked questions about autobiographical information that they answered according to the prompt. Cue-evoked pupillary responses, or the changes in participants' pupils during the fixation period between the prompt and question presentation, served as an objective physiological measure of this preparatory state of attention. To assess cognitive ability, several tasks assessing working memory capacity and attentional control were also administered to determine their relationship with pupil response. Aligned with results from a former study, it was hypothesized that pupil diameter would be greatest in anticipation of "Lie" trials, that working memory capacity and attentional control would be negatively correlated with the proportion of errors committed and positively correlated with pupil size in the final few seconds of the fixation interval, and that pupil diameter variability across the fixation interval would be positively correlated with the proportion of errors committed. Results showed a general pattern of constriction in pupil diameter in the fixation interval, which opposed results from previous studies, and did not provide support for the main hypotheses. Lie trials where participants committed an error displayed a significant decrease in pupil diameter across the fixation interval relative to accurate lie trials. Possible reasons for general pattern of pupil constriction are given, prompting a retesting of the hypotheses under better experimental conditions. It is still possible that there is a general pattern of pupil dilation in this preparatory period.
Investigation of the cellular pathology underlying the optic neuropathy in a mouse model of familial Dysautonomia
(Montana State University - Bozeman, College of Agriculture, 2023) Schultz, Anastasia Mardell; Chairperson, Graduate Committee: R. Steven Stowers; This is a manuscript style paper that includes co-authored chapters.
Familial dysautonomia (FD) is a rare, recessive, progressive autosomal disorder that affects the nervous system. This neurological disorder is caused by a splice mutation in the Elongator complex I (ELP1) gene. The mutation results in a tissue-specific reduction of ELP1 protein due to unstable mRNA targeted for nonsense-mediated decay. ELP1 is a highly conserved scaffolding protein and core subunit of the six-subunit Elongator complex required for normal translation, neuronal development, and survival. Insufficient ELP1 leads to the developmental death of neurons in the peripheral and autonomic nervous systems in addition to central and peripheral nervous system neurodegeneration. Patients suffer from congenital and progressive neuropathies, such as cardiovascular dysfunction, reduced peripheral sensory function, poor growth, and digestive and respiratory problems. Outside of the risk of death in early adulthood, one of the most debilitating conditions affecting patients' quality of life is progressive blindness marked by continual loss of retinal ganglion cells (RGCs). Within the FD community, there is a concerted effort to develop treatments to prevent the loss of RGCs, thereby improving patients' quality of life. This study aims (1) to elucidate mechanisms underlying the death of RGCs in the absence of Elp1 and (2) to obtain pre-clinical intervention data that can eventually be translated into therapeutics for rescuing RGCs in FD. Using histology and confocal microscopy in conjunction with biochemistry, this study provides evidence for disrupted cellular homeostasis and inflammation preceding RGC death, and as the disease progresses, the retinal cells fail to mount a correct stress response to restore neuronal homeostasis. Furthermore, this study provides first-of-its-kind pre-clinical data using targeted gene therapies to rescue RGCs. Understanding the biological crosstalk and signaling mechanisms underlying the death of RGCs in the absence of Elp1 will allow for more targeted and effective therapeutics that will benefit not only the FD community but also individuals affected by other retinal diseases and neurological diseases that result from a faulty Elongator complex. This study provides a novel characterization of the FD retina and establishes baseline methods to further investigate rescuing RGCs.
Macular degeneration, glaucoma, and diabetic retinopathy : a continuing education program
(Montana State University - Bozeman, College of Nursing, 1999) Lewis, Amy Sarah; Chairperson, Graduate Committee: Jean Ballantyne

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