Development of sodium channels during differentiation of chick skeletal muscle in culture. I. Binding studies

Development of sodium channels during differentiation of chick skeletal muscle in culture. I. Binding studies
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培养鸡骨骼肌分化过程中钠通道的发育。

DOI:
10.1523/jneurosci.03-05-00995.1983
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发表时间:
1983
影响因子:
2.7
通讯作者:
I. Spector
I. Spector
中科院分区:
生物学3区
文献类型:
--
作者:
J. Baumgold;J. Parent;I. Spector

文献摘要

被引文献

相似文献

[~(125)I]蝎毒素和[~ 3 H]石房蛤毒素是两种与钠通道不同部位特异性结合的神经毒素。[3 H]石房蛤毒素结合位点在成肌细胞中不可检测。它们仅在成肌细胞融合形成肌管后出现,并逐渐增加,在培养8天时达到最大值58 fmol/mg蛋白质。相比之下,[125 I]蝎毒素结合位点在细胞融合期间首先检测到,并在融合后增加,在培养4天达到最大值,远早于[3 H]石房蛤毒素结合的最大值或完全发达的钠动作电位的出现。[3 H]石房蛤毒素结合和[125 I]蝎毒素结合亲和力在发展过程中都没有变化,它们的值分别为1.4和62 nM。这些数据以及在配套论文(Baumgold,J.,J. B.父母,我。Spector(1983)J. Neurosci.第三章:1004-1013),提示钠通道发育包括两个连续步骤:将能够单独结合蝎毒素的未成熟形式的钠通道掺入细胞膜,随后获得结合石房蛤毒素的能力,从而成为成熟和功能性通道。
[125I]Scorpion toxin and [3H]saxitoxin, two neurotoxins that bind specifically to different sites on sodium channels, were used to monitor the development of sodium channels during synchronous differentiation of chick skeletal muscle in culture. [3H]Saxitoxin- binding sites are not detectable in myoblasts. They appear only after myoblasts fuse to form myotubes and increase gradually to reach a maximal value of 58 fmol/mg of protein by 8 days in culture. In contrast, [125I]scorpion toxin-binding sites are first detected during the period of cell fusion and increase after fusion to reach a maximum by 4 days in culture, well before either the maximal value of the [3H]saxitoxin binding or the appearance of fully developed sodium action potentials. Neither [3H]saxitoxin binding nor [125I] scorpion toxin binding affinity changes during development; they have values of 1.4 and 62 nM, respectively. These data, and data described in the companion paper (Baumgold, J., J. B. Parent, and I. Spector (1983) J. Neurosci. 3: 1004–1013), suggest that sodium channel development involves two sequential steps: incorporation into the cell membrane of an immature form of the sodium channel capable of binding scorpion toxin alone, followed by the acquisition of the ability to bind saxitoxin and thus to become a mature and functional channel.