Moore S E, Walsh F S
Neuroscience. 1986 Jun;18(2):499-505. doi: 10.1016/0306-4522(86)90170-3.
The expression of neural cell adhesion molecule was analysed by indirect immunofluorescence on adult mouse skeletal muscle subjected to a variety of experimental lesions. Adult mouse muscle does not express neural cell adhesion molecule at the sarcolemma. However, following denervation there is a rapid rise in neural cell adhesion molecule levels; this is initially in the cytoplasm of the myofibres but by 18 days there is intense reactivity at the sarcolemma. A nerve crush lesion was used to show that the increase in neural cell adhesion molecule levels following denervation is accompanied by a switch-off of neural cell adhesion molecule expression following reinnervation. Paralysis of skeletal muscle by botulinum toxin injection is sufficient to activate neural cell adhesion molecule expression. As paralysis of skeletal muscle by botulinum toxin is not accompanied by activation of muscle satellite cells or degeneration products of nerve or myelin, it suggests that the observed levels of neural cell adhesion molecule are synthesised by myofibres. As the expression of neural cell adhesion molecule in these lesions parallels the ability of skeletal muscle to accept innervation it is possible that neural cell adhesion molecule acts as a molecular cue at the sarcolemma in regulating synaptogenesis.
通过间接免疫荧光法，对遭受各种实验性损伤的成年小鼠骨骼肌进行神经细胞黏附分子表达分析。成年小鼠肌肉在肌膜处不表达神经细胞黏附分子。然而，去神经支配后神经细胞黏附分子水平迅速升高；最初在肌纤维的细胞质中，到18天时肌膜处出现强烈反应性。使用神经挤压损伤表明，去神经支配后神经细胞黏附分子水平的增加伴随着再支配后神经细胞黏附分子表达的关闭。注射肉毒杆菌毒素使骨骼肌麻痹足以激活神经细胞黏附分子表达。由于注射肉毒杆菌毒素导致骨骼肌麻痹并不伴随着肌肉卫星细胞的激活或神经或髓磷脂的退化产物，这表明观察到的神经细胞黏附分子水平是由肌纤维合成的。由于这些损伤中神经细胞黏附分子的表达与骨骼肌接受神经支配的能力平行，因此神经细胞黏附分子有可能在调节突触形成过程中作为肌膜处的分子信号。
