Defense Date

2009

Document Type

Thesis

Degree Name

Master of Science

Department

Anatomy & Neurobiology

First Advisor

Raymond Colello

Abstract

Multiple sclerosis and other myelin diseases affect the quality of life many people. In the United States alone, multiple sclerosis afflicts as many as 400,000 individuals. Myelin, which is attacked by multiple sclerosis, plays a critical role in maintaining the healthy function of the adult nervous system. There are many model systems that study myelin and its formation and loss. Our lab investigates the cuprizone model of demyelination and remyelination. The cuprizone model is commonly believed only to affect adult oligodendrocytes, which it kills. The current study investigates whether other cells in the oligodendrocyte line, such as oligodendrocyte progenitor cells, might also be susceptible to the toxic effects of cuprizone. Oligodendrocyte progenitor cells may play an important role in repairing and replacing myelin after demyelinating insults. So any effect that the model has on these cells may be relevant to the use of the model for studying remyelination. In order to evaluate the potential effects of cuprizone, dividing cells in adult mice were labeled with the proliferation marker, Bromodeoxyuridine (BrdU). Immunohistochemical labeling of BrdU shows that the number of actively dividing cells seen in the subventricular and subgranular zones sharply and dramatically decreases after just 1 week on cuprizone. In the following weeks, the number of dividing cells increases, but even after 3 weeks of recovery without cuprizone, the number of BrdU+ cells does not return to control levels. These results may have significant ramifications in the interpretation of results obtained from the cuprizone model, and this finding must be considered in selecting a model for future demyelination studies.

Rights

© The Author

Is Part Of

VCU University Archives

Is Part Of

VCU Theses and Dissertations

Date of Submission

June 2009

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