Mechanisms of Calcium Buffering and Aging in Neurons: Testing the Limits of Homeostasis

<p>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.</p>

Name thesis:degree_name

Doctor of Philosophy (PhD)

Level thesis:degree_level

Dissertation

Discipline thesis:degree_discipline

Pharmacology

Year

2000

Author dc:creator

• Pottorf, William James, II

Contributors dc:contributor

• John N. Buchholz
• Sue P. Duckles
• David A. Hessinger
• William J. Pearce
• Lubo Zhang

• Pharmacology
• Calcium -- metabolism; Neurons -- physiology; Homeostasis; Cell Aging.

Statement dc:rights

• 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.

Language dc:language

English

Repository record dc:identifier

https://scholarsrepository.llu.edu/etd/687

OAI identifier oai:identifier

oai:scholarsrepository.llu.edu:etd-1813