Date Approved

2012

Degree Type

Open Access Thesis

Degree Name

Master of Science (MS)

Department

Biology

Committee Member

Robert Winning, PhD, Chair

Committee Member

Geoffrey G. Murphy, PhD, Project Supervisor

Committee Member

Daniel Clemans, PhD

Committee Member

April Liepman, PhD

Abstract

Age-related cognitive decline refers to the memory impairment and difficulty learning new tasks that occurs during the normal process of aging. There are many possible changes that occur at the neuronal level that could account for age-related cognitive decline. One hypothesis suggests that a dysregulation of neuronal intracellular calcium concentration contributes to age-related cognitive deficits. Previous research suggests that an increase in neuronal L-type voltage-gated calcium channels (LVGCCs) occurs in the brain during aging. This increase could account for altered intracellular calcium concentration and lead to agerelated cognitive decline. A line of transgenic mice that over-express the LVGCC CaV1.3 in the forebrain was developed in order to investigate the relative contribution of this change to age-related cognitive decline. These animals were also characterized on both on a molecular and behavioral level. Molecular characterization revealed approximately 20% overexpression of CaV1.3 in the forebrain of transgenic animals, while neurobehavioral experiments indicate these mice have unimpaired motor function and exploratory behaviors. Based upon these results, this new line of mice will be an excellent model for studies of agerelated cognitive decline.

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Updated: 05/24/13

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