Understanding the Origins of Hypersensitivity an a Mouse Model of Duchenne's Muscular Dystrophy

Abstract

Record ID: 224

Award(s): Excellence in Research Mentoring 

Program Affliliation: Ronald E. McNair Post-baccalaureat Acheivement Program; SURF Program (Summer Undergraduate Research Fellowship)

Student Major: Neuroscience

Project Advisor: Michael Jankowski

Abstract: Duchenne's muscular dystrophy (DMD) is a recessive X-linked muscle disease that is rare, but fatal; most patients live until their late 20s or early 30s. DMD causes increasing muscle weakness and eventual loss of use starting from early childhood that stems from alterations to the protein, dystrophin. Though treatments have allotted more time to patients, they do not treat some common symptoms associated with DMD such as pain. The pain associated with DMD significantly decreases the patient's quality of life and often occurs early in disease progression. It is therefore important to understand how pain develops in DMD in order to develop better treatments. We therefore utilized a mouse model of DMD (mdx mouse) which is mutant at the dystrophin gene. We hypothesized that MDX mice will display sensory impairments prior to muscle wasting. We tested various behavioral measures, such as paw guarding, mechanical withdrawal, Rotorod, grip strength, and exercise pressor reflexes (EPR) to assess hypersensitivity over time. We also compared these results to gene expression patterns in the dorsal root ganglia (DRG) of mdx and wildtype (WT) controls. Preliminary results indicate that mdx mice display.