Shainberg A, Cohen S A, Nelson P G
Pflugers Arch. 1976 Feb 24;361(3):255-61. doi: 10.1007/BF00587290.
Acetylcholine receptors in muscle cells differentiated in vitro were monitored by using 125 I-alpha-bungarotoxin. The number of cholinergic receptors was increased 4-8 fold in 2 days due to inhibition of spontaneous contraction of the muscle fibers. The inhibition of this activity, whether mediated through tetrodotoxin, lidocaine or D-600, did not affect the biochemical differentiation of muscle, as represented by creatine-phosphokinase and acetylcholinesterase activity. "Induction" of receptors by tetrodotoxin was inhibited by cycloheximide, actinomycin-D, or 5-bromotubericidine. Dystrophic muscle responded in vitro to inhibition of contraction similar to normal tissue.
利用¹²⁵I-α-银环蛇毒素监测体外分化的肌细胞中的乙酰胆碱受体。由于肌肉纤维自发收缩受到抑制，胆碱能受体数量在2天内增加了4至8倍。这种活性的抑制，无论通过河豚毒素、利多卡因还是D-600介导，均不影响以肌酸磷酸激酶和乙酰胆碱酯酶活性为代表的肌肉生化分化。河豚毒素对受体的“诱导”作用受到环己酰亚胺、放线菌素-D或5-溴尿嘧啶核苷的抑制。营养不良性肌肉在体外对收缩抑制的反应与正常组织相似。
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