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Microglia and calcium dysregulation during chronic neuroinflammation and aging: causes and consequences

Hopp, Sarah Christine
http://rave.ohiolink.edu/etdc/view?acc_num=osu1414416679

Abstract Details

2014, Doctor of Philosophy, Ohio State University, Neuroscience Graduate Studies Program.
Chronic neuroinflammation and aging are key contributors to the pathogenesis and progression of age-associated neurodegenerative diseases. Microglia dysregulation and calcium dysregulation are two shared features of both aging and chronic neuroinflammation. Here, I will describe several studies that systematically dissect the relationship between neuroinflammation, aging, and calcium dysregulation. Chapter 2 describes the neuroinflammatory factors involved with dysregulated microglial activation in aging during an acute intrahippocampal immune challenge. The main finding of Chapter 2 was that aged animals lack post-transcriptional control of pro-inflammatory markers, which may account for microglia dysregulation in aging. Chapter 3 examines the functional consequences of age-associated microglia dysregulation on memory performance during aging and the possible contribution of calcium dysregulation via L-type voltage dependent calcium channels and ryanodine receptors using pharmacological blockade of these two calcium channels. The main finding of Chapter 3 was that blockade of these two calcium channels differentially improved memory, and that reduced ryanodine receptor expression may protect memory function in aging. In order to examine the specific interaction between neuroinflammation and calcium dysregulation via L-type voltage dependent calcium channels and ryanodine receptors, Chapters 4 and 5 utilize a model of experimentally-induced chronic neuroinflammation in young rats as well as pharmacological treatment to block the two aforementioned calcium channels. Chapter 4 specifically examined the hippocampus and memory alterations induced by chronic neuroinflammation, and found that L-type voltage dependent calcium channels drive calcium dysregulation and memory deficits during chronic neuroinflammation. Chapter 5 specifically examined the brainstem monoaminergic nuclei and motor behavior alterations induced by chronic neuroinflammation, and found that calcium dysregulation plays a differential role in the locus coeruleus and substantia nigra. Finally, Chapter 6 summarizes the main conclusions of this dissertation and presents future avenues of research.
Wenk Gary (Advisor)
279 p.
Neurosciences
microglia; aging; calcium; calcium dysregulation; ryanodine receptors; L-type voltage dependent calcium channels; neuroinflammation; memory; substantia nigra; locus coeruleus; hippocampus; cytokines; neuroimmunology; behavioral neuroscience

Recommended Citations

Citations

  • Hopp, S. C. (2014). Microglia and calcium dysregulation during chronic neuroinflammation and aging: causes and consequences [Doctoral dissertation, Ohio State University]. OhioLINK Electronic Theses and Dissertations Center. http://rave.ohiolink.edu/etdc/view?acc_num=osu1414416679

    APA Style (7th edition)

  • Hopp, Sarah. Microglia and calcium dysregulation during chronic neuroinflammation and aging: causes and consequences. 2014. Ohio State University, Doctoral dissertation. OhioLINK Electronic Theses and Dissertations Center, http://rave.ohiolink.edu/etdc/view?acc_num=osu1414416679.

    MLA Style (8th edition)

  • Hopp, Sarah. "Microglia and calcium dysregulation during chronic neuroinflammation and aging: causes and consequences." Doctoral dissertation, Ohio State University, 2014. http://rave.ohiolink.edu/etdc/view?acc_num=osu1414416679

    Chicago Manual of Style (17th edition)

osu1414416679
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This open access ETD is published by The Ohio State University and OhioLINK.