Neurology
HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS
 QUICK SEARCH:   [advanced]


     


This Article
Right arrow Full Text (PDF)
Right arrow Correspondence:
Submit a response
Right arrow Alert me when this article is cited
Right arrow Alert me when Correspondence are posted
Right arrow Alert me if a correction is posted
Services
Right arrow Email this article to a friend
Right arrow Similar articles in this journal
Right arrow Similar articles in PubMed
Right arrow Alert me to new issues of the journal
Right arrow Download to citation manager
Right arrow reprints & permissions
Citing Articles
Right arrow Citing Articles via HighWire
Right arrow Citing Articles via Google Scholar
Google Scholar
Right arrow Articles by LINDSTROM, J. M.
Right arrow Articles by LAMBERT, E. H.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by LINDSTROM, J. M.
Right arrow Articles by LAMBERT, E. H.
NEUROLOGY 1978;28:130
© 1978 American Academy of Neurology

Content of acetylcholine receptor and antibodies bound to receptor in myasthenia gravis, experimental autoimmune myasthenia gravis, and Eaton-Lambert syndrome

JON M. LINDSTROM, Ph.D. and EDWARD H. LAMBERT, M.D.

Salk Institute for Biological Studies, San Diego, California (Dr. Lindstrom), and the Mayo Clinic and Mayo Foundation, Rochester, Minnesota.

The acetylcholine receptor content of intercostal muscle biopsies from patients with myasthenia gravis is reduced, and many of the remaining receptors have antibodies bound to them. Decreased receptor content and inhibition of receptor activity by bound antibodies can account for the reduced amplitude of the miniature endplate potential in these patients. Patients with Eaton-Lambert syndrome, who release reduced numbers of acetylcholine quanta, have normal receptor content and miniature endplate potential amplitude, and do not have antibodies bound to their receptors. As the severity of myasthenia gravis increases, the content of receptor remaining unbound by antibody decreases, as does miniature endplate potential amplitude. Similar decreases in receptor content and similar concentrations of antibody-labeled receptor are found in rats with experimental autoimmune myasthenia gravis. Regardless of the severity of their myasthenia, receptor content in rats does not decrease much below 40 percent of normal, and increasing weakness is associated with the binding of antibodies to an increasing fraction of the remaining receptors. In both myasthenia gravis and its animal model, a decrease in the content of fully active receptor is probably the most important factor impairing neuromuscular transmission. Pathologic mechanisms responsible for decreased receptor content and alteration of postsynaptic membrane morphology are discussed.

Address reprint requests to Dr. Lindstrom, Salk Institute for Biological Studies, P.O. Box 1809, San Diego, CA 92112.

This work was supported by NIH research grant NS 11323 to Dr. Lindstrom; by a research grant from the Muscular Dystrophy Association to Dr. Lindstrom; and by a Center Grant from the Muscular Dystrophy Association to Dr. Lambert.

Accepted for publication May 23, 1977.




This article has been cited by other articles:


Home page
Palliat MedHome page
R. Grant
Nonmetastatic manifestations of malignancy: neurological
Palliative Medicine, July 1, 1989; 3(3): 181 - 188.
[Abstract] [PDF]


Home page
Cold Spring Harb Symp Quant BiolHome page
J. Lindstrom, S. Tzartos, W. Gullick, S. Hochschwender, L. Swanson, P. Sargent, M. Jacob, and M. Montal
Use of Monoclonal Antibodies to Study Acetylcholine Receptors from Electric Organs, Muscle, and Brain and the Autoimmune Response to Receptor in Myasthenia Gravis
Cold Spring Harb Symp Quant Biol, January 1, 1983; 48(0): 89 - 99.
[Abstract] [PDF]




HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS
Copyright © 1978 by AAN Enterprises, Inc.