Intracellular calcium ([Ca2+]i) is an ubiquitous second messenger that integrates multiple and diverse neuronal pathways that include development and maturation, gene expression, synaptic plasticity, transmitter release, excitability, and even cell death. Upon neuronal excitation the [Ca2+]i increases rapidly and the calcium buffering system reacts quickly to restore [Ca2+]i to basal levels in order to reset the cell for the next stimulus and avoid prolonged exposure to cytotoxic levels of high [Ca2+]i. The aging process appears to causes multiple changes in the ability of neurons to regulate [Ca2+]i homeostasis and an age-related breakdown in the mechanisms controlling [Ca2+]i homeostasis could contribute to decreased neuronal function or neurodegeneration. Thus, it is hypothesized that the aging process results in decreased function of sarco/endoplasmic reticulum calcium ATPase (SERCA) pumps, leading to greater or more sustained [Ca2+]i levels, an increased reliance on remaining calcium buffering components to restore [Ca2+]i homeostasis and regulate neurotransmitter release in adrenergic neurons.
John N. Buchholz
Sue P. Duckles
David A. Hessinger
William J. Pearce
Doctor of Philosophy (PhD)
Year Degree Awarded
Date (Title Page)
Library of Congress/MESH Subject Headings
Calcium -- metabolism; Neurons -- physiology; Homeostasis; Cell Aging.
Loma Linda University Libraries
This title appears here courtesy of the author, who has granted Loma Linda University a limited, non-exclusive right to make this publication available to the public. The author retains all other copyrights.
Pottorf, William James II, "Mechanisms of Calcium Buffering and Aging in Neurons: Testing the Limits of Homeostasis" (2000). Loma Linda University Electronic Theses, Dissertations & Projects. 687.
Loma Linda University Electronic Theses and Dissertations
Loma Linda University. Del E. Webb Memorial Library. University Archives