3,4-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)
The University of North Carolina at Pembroke (UNCP )
Web Site: http://www.uncp.edu/academics/library
Robert Poage

Abstract: Lambert-Eaton Myasthenic Syndrome (LEMS) is a debilitating autoimmune disease where the neuromuscular junction (NMJ) 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 potentials. Since presynaptic action potentials are broadened, more influx of calcium through VGCC occurs, and additional acetylcholine 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 simulate 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) generated 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

Honors Project
Esther G. Maynor Honors College
Language: English
Date: 2019
Lambert-Eaton Myasthenic Syndrome (LEMS), autoimmune, neuromuscular junction (NMI), voltage-gated calcium channels (BFCC), acetylcholine, 3,4-Diaminopyridine (3, 4-DAP), presynaptic potassium channels, presynaptic action potentials, muscle contractability

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