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- Genre: Doctoral Dissertation
Description
Cognitive function is multidimensional and complex, and research indicates that it is impacted by age, lifetime experience, and ovarian hormone milieu. One particular domain of cognitive function that is susceptible to age-related decrements is spatial memory. Cognitive practice can affect spatial memory when aged in both males and females, and in females alone ovarian hormones have been found to alter spatial memory via modulating brain microstructure and function in many of the same brain areas affected by aging. The research in this dissertation has implications that promote an understanding of the effects of cognitive practice on aging memory, why males and females respond differently to cognitive practice, and the parameters and mechanisms underlying estrogen's effects on memory. This body of work suggests that cognitive practice can enhance memory when aged and that estrogen is a probable candidate facilitating the observed differences in the effects of cognitive practice depending on sex. This enhancement in cognitive practice effects via estrogen is supported by data demonstrating that estrogen enhances spatial memory and hippocampal synaptic plasticity. The estrogen-facilitated memory enhancements and alterations in hippocampal synaptic plasticity are at least partially facilitated via enhancements in cholinergic signaling from the basal forebrain. Finally, age, dose, and type of estrogen utilized are important factors to consider when evaluating estrogen's effects on memory and its underlying mechanisms, since age alters the responsiveness to estrogen treatment and the dose of estrogen needed, and small alterations in the molecular structure of estrogen can have a profound impact on estrogen's efficacy on memory. Collectively, this dissertation elucidates many parameters that dictate the outcome, and even the direction, of the effects that cognitive practice and estrogens have on cognition during aging. Indeed, many parameters including the ones described here are important considerations when designing future putative behavioral interventions, behavioral therapies, and hormone therapies. Ideally, the parameters described here will be used to help design the next generation of interventions, therapies, and nootropic agents that will allow individuals to maintain their cognitive capacity when aged, above and beyond what is currently possible, thus enacting lasting improvement in women's health and public health in general.
ContributorsTalboom, Joshua S (Author) / Bimonte-Nelson, Heather A. (Thesis advisor) / Conrad, Cheryl D. (Committee member) / Neisewander, Janet L (Committee member) / West, Stephen G. (Committee member) / Arizona State University (Publisher)
Created2011
Description
Neurotoxicology has historically focused on substances that directly damage nervous tissue. Behavioral assays that test sensory, cognitive, or motor function are used to identify neurotoxins. But, the outcomes of behavioral assays may also be influenced by the physiological status of non-neural organs. Therefore, toxin induced damage to non- neural organs may contribute to behavioral modifications. Heavy metals and metalloids are persistent environmental pollutants and induce neurological deficits in multiple organisms. However, in the honey bee, an important insect pollinator, little is known about the sublethal effects of heavy metal and metalloid toxicity though they are exposed to these toxins chronically in some environments. In this thesis I investigate the sublethal effects of copper, cadmium, lead, and selenium on honey bee behavior and identify potential mechanisms mediating the behavioral modifications. I explore the honey bees’ ability to detect these toxins, their sensory perception of sucrose following toxin exposure, and the effects of toxin ingestion on performance during learning and memory tasks. The effects depend on the specific metal. Honey bees detect and reject copper containing solutions, but readily consume those contaminated with cadmium and lead. And, exposure to lead may alter the sensory perception of sucrose. I also demonstrate that acute selenium exposure impairs learning and long-term memory formation or recall. Localizing selenium accumulation following chronic exposure reveals that damage to non-neural organs and peripheral sensory structures is more likely than direct neurotoxicity. Probable mechanisms include gut microbiome alterations, gut lining
damage, immune system activation, impaired protein function, or aberrant DNA methylation. In the case of DNA methylation, I demonstrate that inhibiting DNA methylation dynamics can impair long-term memory formation, while the nurse-to- forager transition is not altered. These experiments could serve as the bases for and reference groups of studies testing the effects of metal or metalloid toxicity on DNA methylation. Each potential mechanism provides an avenue for investigating how neural function is influenced by the physiological status of non-neural organs. And from an ecological perspective, my results highlight the need for environmental policy to consider sublethal effects in determining safe environmental toxin loads for honey bees and other insect pollinators.
damage, immune system activation, impaired protein function, or aberrant DNA methylation. In the case of DNA methylation, I demonstrate that inhibiting DNA methylation dynamics can impair long-term memory formation, while the nurse-to- forager transition is not altered. These experiments could serve as the bases for and reference groups of studies testing the effects of metal or metalloid toxicity on DNA methylation. Each potential mechanism provides an avenue for investigating how neural function is influenced by the physiological status of non-neural organs. And from an ecological perspective, my results highlight the need for environmental policy to consider sublethal effects in determining safe environmental toxin loads for honey bees and other insect pollinators.
ContributorsBurden, Christina Marie (Author) / Amdam, Gro (Thesis advisor) / Smith, Brian H. (Thesis advisor) / Gallitano-Mendel, Amelia (Committee member) / Harrison, Jon (Committee member) / Vu, Eric (Committee member) / Arizona State University (Publisher)
Created2016