Neuromuscular junction as Achilles' heel
Yet another autoantibody?
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Every contraction of skeletal muscle entails the release of acetylcholine (ACh) from the motor nerve terminal, its passage across a submicroscopic space, and combination with the postsynaptic ACh receptors (AChRs), which in turn triggers the events of muscle contraction. This tiny movement of ACh across a 70-nM gap not only is highly complex but is vulnerable to a wide variety of attacks or errors that may cause weakness or paralysis. Some examples include bacteria (8 different botulinum toxins, tetanus toxin), plants (curare), snakes (cobratoxin, bungarotoxin), black widow spiders (latrotoxin), frogs (histrionicotoxin), and, of course, humans (anti-cholinesterase war gases sarin, tabun).
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Letters: Rapid online correspondence
- Re:Neuromuscular junction as Achilles' heel: Yet another autoantibody?
- Daniel B. Drachman, Professor, Johns Hopkins School of Medicinedandrac@aol.com
- Henry J. Kaminski, Washington D.C.
Submitted October 31, 2014 - Neuromuscular junction as Achilles' heel: Yet another autoantibody?
- Robert P. Lisak, MD, FAAN, FRCP (UK), FANA, Parker Webber Chair in Neurology Professor of Neurology Professor of Immunology and Microbiology, Wayne State Universityrlisak@med.wayne.edu
- Bin Zhang, Wuhan, China; Chengyong Shen, Lin Mei, Augusta, Georgia
Submitted July 07, 2014
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