Publication Date

2020

Document Type

Thesis

Committee Members

Andrew Voss, Ph.D. (Advisor); Mark Rich, M.D., Ph.D. (Committee Member); Lynn Hartzler, Ph.D. (Committee Member)

Degree Name

Master of Science (MS)

Abstract

In this thesis, we develop a system to study in vivo muscle function in a mouse model of Huntington’s disease that allows for the recording of muscle force by stimulating the motor nerves or the muscles directly after a nerve block. This allows us to distinguish between defects in the nerve, such as problems with vesicle release, and primary muscle defects, such as altered intracellular calcium homeostasis. We hypothesize that there are primary defects in R6/2 skeletal muscle that are separate from neurodegeneration or defects in the CNS. In this case, we should see defects in muscle force generation during nerve stimulation and direct muscle stimulation. If our hypothesis is shown to be correct, this work would highlight new targets to study for the treatment of HD. Peripheral treatments of skeletal muscle are a promising area for the treatment of HD as motor defects are debilitating for patients.

Page Count

82

Year Degree Awarded

2020

ORCID ID

0000-0001-9167-3806


Included in

Biology Commons

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