Density and distribution of alpha-bungarotoxin-binding sites in postsynaptic structures of regenerated rat skeletal muscle.
Density and distribution of alpha-bungarotoxin-binding sites in postsynaptic structures of regenerated rat skeletal muscle.
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DOI：
10.1083/jcb.88.2.338
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发表时间：
1981-02
影响因子：
7.8
通讯作者：
Bader, D
中科院分区：
文献类型：
--
作者：
Bader, D
乙酰胆碱受体 (AChR) 在脊椎动物骨骼肌的突触后区域以离散且可预测的方式组织。当肌肉受损时，神经和肌纤维（包括终板的肌肉成分）会退化，但结缔组织成分会存活。肌纤维在原始肌纤维的基底层内再生。再生哺乳动物骨骼肌的突触后分化可以以不同的方式发生：（a）在存在或不存在神经的情况下在原始终板的位置，或（b）在存在神经的情况下当原始终板不存在时在再生肌纤维的异位区域。本研究使用(125)I-α-银环蛇毒素((125)I-α-BuTX)和电镜放射自显影检查在没有神经的情况下原始终板部位再生的突触后结构中以及在去除原始终板时在有神经存在的情况下肌纤维异位部位再生的突触后结构中AChR的密度和分布。在再生肌纤维中，α-BuTX 结合位点的密度落在未受伤肌肉中观察到的密度范围内，无论突触后分化发生在没有神经的原始终板部位还是再生肌纤维的原始异位位置。此外，再生突触后区域内α-BuTX结合位点的分布与未受伤肌肉中apha-BuTX结合位点的分布非常相似。对在没有神经的情况下在原始终板部位形成的突触后结构或通过神经和肌肉的相互作用在再生肌纤维的异位位置处形成的突触后结构进行形态测量分析。尽管原发裂的深度发生了变化，但再生的突触后结构的整体结构与未受伤肌肉终板的结构之间几乎没有差异。
Acetylcholine receptors (AChR) are organized in a discrete and predictable fashion in the postsynaptic regions of vertebrate skeletal muscle. When muscle is damaged, nerves and myofibers including muscular elements of the endplate degenerate, but the connective tissue elements survive. Muscle fibers regenerate within the basal lamina of the original myofiber. Postsynaptic differentiation in regenerated mammalian skeletal muscle can occur in different ways: (a) at the site of the original endplate in the presence or absence of the nerve, or (b) at ectopic regions of the regenerated myofiber in the presence of the nerve when the original endplate is not present. The present study used (125)I-α- bungarotoxin ((125)I-α-BuTX) and EM autoradiography to examine the density and distribution of AChR in postsynaptic structures regenerated at the site of the original endplate in the absence of the nerve and at ectopic sites of the myofiber in the presence of the nerve when the original endplate was removed. In regenerated myofibers, the density of α-BuTX-binding sites fell within the range of densities observed in uninjured muscle whether postsynaptic differentiation occurred at the site of the original endplate in the absence of the nerve or at an originally ectopic position of the regenerated myofiber. In addition, the distribution of α-BuTX-binding sites within the regenerated postsynaptic regions closely resembled the distribution of apha-BuTX- binding sites in uninjured muscle. Morphometric analysis was performed on postsynaptic structures formed at the site of the original endplate in the absence of the nerve or at an ectopic position of the regenerated myofiber by interaction of the nerve and muscle. Although variation in the depth of the primary cleft occurred, there was little difference between the overall structure of regenerated postsynaptic structures and that of endplates of uninjured muscles.