Research Symposium

26th annual Undergraduate Research Symposium, April 1, 2026

Madisen Clark Poster Session 2: 10:45 am - 11:45 am / Poster #90


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BIO


Madisen Clark is a second-year undergraduate pursuing dual B.S. degrees in Cell & Molecular Neuroscience and Linguistics & Modern Languages, with minors in Chemistry and Spanish. Through the Undergraduate Research Opportunity Program (UROP), she assists research in Dr. Brown’s lab studying muscle atrophy and metabolic disease. She is also an Honors Directed Individual Study (DIS) student in the Learning, Memory, and Language Lab with Dr. Kaschak, assisting with psycholinguistic research on conversational turn-taking dynamics. On campus, Madisen is actively involved in several organizations, including Phi Delta Epsilon Medical Fraternity, the FSU Medical Response Unit, Club Tennis, the FSU Honors Student Association, and Medical Brigades, where she has had the honor of serving on the executive board this academic year. Off campus, she volunteers with Big Bend Hospice at Tallahassee Memorial Hospital and works part-time as a medical assistant at a local allergy clinic. After completing her undergraduate studies, Madisen plans to attend medical school and pursue a career as a physician.

Disuse-Atrophy Exacerbates Denervation in Aged Rats

Authors: Madisen Clark, Jacob Brown
Student Major: Cell & Molecular Neuroscience and Linguistics & Modern Languages
Mentor: Jacob Brown
Mentor's Department: Exercise Physiology
Mentor's College: College of Health and Human Sciences
Co-Presenters: Alyssa L. Moodie, Kaitlyn R. Harrison, Ava J. Sajovits, Catherine Zhou

Abstract


Older humans fail to recover skeletal muscle mass and function after muscle loss due to bedrest, which contrasts with young and adult humans, leading to muscle loss and an increase in morbidity and mortality in the aged population. Disorders disrupting the neuromuscular junction, the synapse where motor nerves meet muscles, are associated with age-related muscle atrophy and dysfunction. We hypothesized that periods of disuse-atrophy will exacerbate neuromuscular pathologies in aged rats. 28-month-old rats were hindlimb unloaded, a condition where the rats cannot put weight on their hindlimbs, for 14 days to induce disuse atrophy. 28-month-old weight-bearing rats were used as controls. Muscle wet weights were measured at sacrifice. Via immunofluorescence, we assessed acetyl choline receptor endplate area, acetyl choline receptor endplate fragmentation, and denervation of the neuromuscular junctions. Oxylipins, oxidized lipid signaling molecules, were measured in gastrocnemius muscle. We performed a student’s t-test for statistical analysis. Muscle wet weights were 20-40% lower in rats that were hindlimb-unloaded compared to controls. Acetyl choline receptor area and fragmentation were 20% higher in gastrocnemius from hindlimb-unloaded rats compared to controls. Denervation was 30% higher in the gastrocnemius from hindlimb-unloaded rats compared to controls. The muscle oxylipin profile in aged weight-bearing and adult hindlimb-unloaded rats were significantly altered when compared to adult weight-bearing rats. However, muscle oxylipin profile was not different when comparing aged and aged hindlimb unloaded muscle. These data show that hindlimb-unloading exacerbates neuromuscular pathologies in aged rats. Therapies that protect neuromuscular junctions may help improve recovery following disuse-atrophy in aged subjects.

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Keywords: Disuse-atropy, neuromuscular junction, muscular atrophy