小鼠骨胳肌在切腱、协同肌切腱和肉毒杆菌毒素中毒后对辣根过氧化物酶(HRP)的胞纳作用

本文报道了用生物化学方法测定离体小鼠比目鱼肌对 HRP 的胞纳作用。结果表明,在切断神经或切腱后引起萎缩的肌肉侧或在协同肌切腱后引起代偿性肥大的肌肉侧,与它们各自对照的正常肌肉侧相比,都可发生对 HRP 胞纳的明显增加。而在肉毒杆菌毒素中毒后引起萎缩的肌肉侧,和它正常的对照肌肉侧相比,却意外地不发生这种胞纳摄取的明显增加。本文的实验结果进一步证实。肌肉的胞纳增加并不一定导致肌纤维的变性和萎缩(例如代偿性肥大的肌肉);而肌纤维的变性和萎缩亦不一定需要肌肉的胞纳增加为前提(例如肉毒杆菌毒素中毒的肌肉)。本工作结果还提示:肌肉的胞纳增加有其神经原性和肌原性因素。本文还对肌肉胞纳增加的可能机制进行了讨论。

ENDOCYTOSIS OF HORSERADISH PEROXIDASE(HRP)IN MOUSE SKELETAL MUSCLE AFTER TENOTOMY,TENOTOMY OF SYNERGISTIC MUSCLE AND BOTULINUM POISONING

Endocytized uptake of horseradish peroxidase(HRP)in mouse soleus musclein vitro was determined by biochemical method.Our results clearly showed an increased uptake of HRP present in denervatedmuscle,tenotomized muscle and tenotomized muscle of synergistic muscle ascompared with respective control muscle.No significant difference in the uptake of HRP was found between botulinumpoisoned and contralateral control muscles.The results of the above experiments suggest that enhanced endocytosis doesnot necessarily result in muscle fiber degeneration and atrophy(such as compensa-tive hypertrophic muscle)and that degeneration and atrophy of muscle fiber maynot require increase of endocytosis as a premise or inducer(such as botulinumpoisoned muscle).The possible mechanism for the enhancement of endocytosis in muscle fiberwas discussed.