Increases in muscle Ca2+ mediate changes in acetylcholinesterase and acetylcholine receptors caused by muscle contraction.
Increases in muscle Ca2+ mediate changes in acetylcholinesterase and acetylcholine receptors caused by muscle contraction.
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肌肉 Ca2 的增加介导肌肉收缩引起的乙酰胆碱酯酶和乙酰胆碱受体的变化。
DOI：
10.1073/pnas.82.20.7121
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发表时间：
1985
影响因子：
11.1
通讯作者：
L. Rubin
中科院分区：
文献类型：
--
作者：
L. Rubin
通过培养的大鼠肌纤维合成乙酰胆碱酯酶（AcChoE;乙酰胆碱乙酰水解酶，EC 3.1.1.7）和乙酰胆碱受体（AcChoR）受到肌肉收缩活性水平的强烈影响。如果纤维生长在河豚毒素（TTX）的存在下，以阻止自发收缩，乙酰胆碱酯酶的总量显着减少，因为乙酰胆碱酯酶的百分比组装为胶原尾假定的突触形式的酶。然而，在这些条件下，AcChoR的数量增加。我们在这里证明，TTX的每一个效果都可以通过用钙离子载体A23187处理肌细胞来预防。因此，与单独在TTX中生长的细胞相比，用A23187和TTX处理的细胞具有高30至40倍的胶原尾化AcChoE水平和低4-5倍的AcChoR水平。这些结果表明，增加肌肉细胞质Ca 2+介导的已知的影响，肌肉收缩对这些胆碱能大分子。
The synthesis of acetylcholinesterase (AcChoE; acetylcholine acetylhydrolase, EC 3.1.1.7) and of acetylcholine receptors (AcChoR) by cultured rat muscle fibers is influenced strongly by the level of muscle contractile activity. If fibers are grown in the presence of tetrodotoxin (TTX) to block spontaneous contraction, the total amount of AcChoE decreases markedly, as does the percentage of AcChoE assembled as the collagen-tailed presumed synaptic form of the enzyme. Under these conditions, however, the number of AcChoR increases. We demonstrate here that each effect of TTX can be prevented by treating the muscle cells with the calcium ionophore A23187. Thus, cells treated with A23187 and TTX have 30- to 40-fold higher levels of collagen-tailed AcChoE and lower levels of AcChoR by a factor of 4-5 than do cells grown in TTX alone. These results suggest that an increase in muscle cytoplasmic Ca2+ mediates the known effects of muscle contraction on these cholinergic macromolecules.