Connold A L, Kamel-Reid S, Vrbová G, Zak R
Department of Anatomy and Developmental Biology, University College London, UK.
Pflugers Arch. 1993 Apr;423(1-2):34-40. doi: 10.1007/BF00374958.
Denervation of the anterior latissimus dorsi (ALD) muscle causes transient muscle fibre hypertrophy and leads to an increase of the SM1 myosin isoform. We tested whether the changes that take place after denervation can be attributed to loss of muscle activity which follows denervation. Neuromuscular activity was prevented by blocking the acetylcholine receptors with alpha-bungarotoxin and thereby paralysing the muscle. Following this treatment, we found increased muscle weight and pronounced hypertrophy of muscle fibres. Also, the proportion of SM1 isomyosin was decreased. Due to the multiple innervation of ALD muscle fibres it is possible to paralyze only part of the muscle. When only a region of the muscle was paralysed a local hypertrophy of fibres was detected, and the change from SM1 to SM2 was most pronounced in the area where activity was blocked. Removal of muscle activity resulted in changes similar to those that occurred after denervation.
背阔肌前肌（ALD）去神经支配会导致肌肉纤维短暂肥大，并导致SM1肌球蛋白亚型增加。我们测试了去神经支配后发生的变化是否可归因于去神经支配后肌肉活动的丧失。通过用α-银环蛇毒素阻断乙酰胆碱受体从而使肌肉麻痹来防止神经肌肉活动。经过这种处理后，我们发现肌肉重量增加且肌肉纤维明显肥大。此外，SM1同工型肌球蛋白的比例降低。由于ALD肌肉纤维有多重神经支配，因此有可能仅使部分肌肉麻痹。当仅使肌肉的一个区域麻痹时，检测到纤维局部肥大，并且从SM1到SM2的变化在活动被阻断的区域最为明显。去除肌肉活动导致的变化与去神经支配后发生的变化相似。
