Noble M D, Brown T H, Peacock J H
Neurosci Lett. 1979 Feb;11(2):149-54. doi: 10.1016/0304-3940(79)90118-6.
Long term (24--96 h) treatment of a mouse-derived myogenic cell line (G8) with meostigmine or physostigmine markedly reduces binding of alpha-bungarotoxin (alpha-BuTx) to these cells. Protein synthesis in these cultures is markedly reduced and cell morphology degenerates. Myotubes maintain slightly hyperpolarised resting membrane potentials, and are able to respond to iontophoretic acetylcholine (ACh) application with overshooting action potentials. Prolonged exposure to neostigmine also inhibits protein synthesis in a fibroblastic cell line (B82). The results suggest that degenerative changes at the neuromuscular junction associated with chronic neostigmine treatment in vivo are due to a direct action of the anticholinesterase on the muscle, rather than to altered intracleft ACh levels [2] or to presynaptic effects of the anticholinesterase [15].
用新斯的明或毒扁豆碱对小鼠源成肌细胞系(G8)进行长期(24 - 96小时)处理,可显著降低α-银环蛇毒素(α-BuTx)与这些细胞的结合。这些培养物中的蛋白质合成显著减少,细胞形态发生退化。肌管维持轻度超极化的静息膜电位,并且能够对离子电泳施加的乙酰胆碱(ACh)产生超射动作电位反应。长期暴露于新斯的明也会抑制成纤维细胞系(B82)中的蛋白质合成。结果表明,体内与慢性新斯的明治疗相关的神经肌肉接头处的退行性变化是由于抗胆碱酯酶对肌肉的直接作用,而非由于裂隙内乙酰胆碱水平的改变[2]或抗胆碱酯酶的突触前效应[15]。