In:
Annals of Neurology, Wiley, Vol. 37, No. 5 ( 1995-05), p. 627-636
Abstract:
In myasthenia gravis, loss of acetylcholine receptors at motor end‐plates is induced by antireceptor autoantibodies. At end‐plates in rats in which myasthenia gravis–like symptoms are induced by chronic treatment with α‐bungarotoxin, acetylcholine release is increased. Within muscles from such rats there is a strong correlation between the increase of acetylcholine release at an end‐plate and the loss of postsynaptic acetylcholine receptors, caused by the toxin. The question is whether upregulation of acetylcholine release is a clinically relevant compensatory mechanism in myasthenia gravis or only a feature of the animal model using α‐bungarotoxin. We investigated electrophysiologically the in vitro acetylcholine release at end‐plates of muscles from patients with myasthenia gravis and rats with experimental autoimmune myasthenia gravis where acetylcholine receptor reduction is caused by autoantibody attack. In both human and rat autoimmune myasthenic muscle, the mean quantal content was considerably increased compared with control levels. At each individual myasthenic end‐plate, the increase in quantal content appeared to be correlated with the reduction of the amplitude of the miniature end‐plate potential. This finding suggests the existence of an important compensatory mechanism in myasthenia gravis, in which retrograde acting factors (i.e., from muscle fiber to nerve terminal) upregulate acetylcholine release.
Type of Medium:
Online Resource
ISSN:
0364-5134
,
1531-8249
DOI:
10.1002/ana.410370513
Language:
English
Publisher:
Wiley
Publication Date:
1995
detail.hit.zdb_id:
2037912-2
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