HUMAN MYASTHENIC SERA REDUCE ACETYLCHOLINE SENSITIVITY OF HUMAN MUSCLE-CELLS IN TISSUE-CULTURE
HUMAN MYASTHENIC SERA REDUCE ACETYLCHOLINE SENSITIVITY OF HUMAN MUSCLE-CELLS IN TISSUE-CULTURE
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DOI：
10.1038/267263a0
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发表时间：
1977-01-01
期刊：
影响因子：
64.8
通讯作者：
HEINEMANN, SF
中科院分区：
文献类型：
--
作者：
BEVAN, S;KULLBERG, RW;HEINEMANN, SF
MYASTHENIA gravis is a muscle disease of man characterised by impaired neuromuscular transmission during repetitive motor nerve activity. Recent studies suggest that the defect in myasthenia gravis is post-synaptic and that myasthenic end-plates have a lower density of functional acetylcholine (ACh) receptors than normal end-plates. Thus end-plates from myasthenic patients show unusually small miniature end-plate potentials1,2, are less sensitive than normal end-plates to iontophoretically applied ACh (refs 2, 3) and bind reduced amounts of α-bungarotoxin4,5—a snake neurotoxin which is considered to bind specifically to nicotinic ACh receptors (see ref. 5). The presence of antibodies against ACh receptors in the sera of myasthenic but not of control patients6–10suggests that anti-receptor antibodies might act in some way to decrease the number of functional receptors at the motor end-plate. Previous investigations, however, have failed to show conclusively that myasthenic sera contain a factor that reduces muscle ACh sensitivity3,11–13. Here we show that myasthenic sera can reduce the ACh sensitivity of tissue cultured human muscle cells.
