34-Diaminopyridine as a Treatment for Lambert-Eaton Myasthenic Syndrome (LEMS)

UNCP Author/Contributor (non-UNCP co-authors, if there are any, appear on document)
Savannah Melvin (Creator)
Institution
The University of North Carolina at Pembroke (UNCP )
Web Site: http://www.uncp.edu/academics/library
Advisor
Robert Poage

Abstract: Lambert-Eaton Myasthenic Syndrome (LEMS) is a debilitating autoimmune disease where the neuromuscular junction(NMI) does not function normally. A patient with LEMS has damaged voltage-gated calcium channels (VGCC), which in return does not allow their NMJ to release an adequate amount of acetylcholine for muscle contraction. A novel treatment for LEMS is administering 3,4-Diaminopyridine (3,4-DAP), because the drug blocks presynaptic potassium channels and broadens presynaptic action potentias. Since presynaptic action potentials are broadened, more influx of calcium throug VGCC occurs, and additional acetylchline is released, reducing the muscle weakness associated with LEMS. To further LEMS research, we used a frog model (gastrocnemius muscle and the sciatic nerve). The frog muscle and nerve were soaked in different calcium concentrations to stimulate LEMS. After we collected control data, we treated the muscle-nerve preparation with 3,4-DAP and investigated the effects 3,4-DAP has on muscle excitability and nerve excitability. We predicted that muscle twitch (force) generate by nerve stimulation would be enhanced by 3,4-DAP treatment but that direct muscle stimulation would be unaffected. We find that the research supports our original hypothesis.

Additional Information

Publication
Honors Project
Language: English
Date: 2019
Keywords
Lambert-Eaton Myasthenic Syndrome, Autoimmune disease, Nuermuscular Junction, Voltage-gated Calcium Channels, 3,4-Diaminopyridine,

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