Morgan J E
Department of Histopathology, Charing Cross and Westminster Medical School, London, U.K.
J Neurol Sci. 1988 Sep;86(2-3):149-58. doi: 10.1016/0022-510x(88)90094-9.
In the course of work in which the phosphorylase kinase (PhK)-deficient mouse was used as a model of a defined inherited myopathy, we measured the PhK activity in regenerated autografts of normal whole extensor digitorum longus (EDL) muscles. Initially, no PhK activity was found for up to 71 days after grafting. A more sensitive assay technique revealed PhK activity in regenerated normal grafts from 43 days after grafting, but the levels never reached those found in ungrafted normal muscle. PhK activity was also reduced in normal EDL muscles following either: denervation, or tenotomy, or denervation and devascularisation, or denervation, devascularisation and tenotomy, but the reduction was never as great as that observed in grafted muscle of equivalent age. PhK activity was also reduced in the tibialis anterior (TA) muscles of the myopathic C57B1/10 mdx strain of mouse, in which the skeletal muscles undergo persistent bouts of degeneration and regeneration, whilst retaining their vascular and nervous connections. It was concluded that the loss of PhK activity in grafted muscle is due to a combination of the effects of denervation, tenotomy and regeneration which occur on grafting.
在以磷酸化酶激酶（PhK）缺陷型小鼠作为特定遗传性肌病模型的研究工作中，我们测量了正常趾长伸肌（EDL）肌肉自体移植再生后的PhK活性。最初，移植后长达71天均未检测到PhK活性。一种更灵敏的检测技术显示，从移植后43天起，再生的正常移植组织中出现了PhK活性，但活性水平从未达到未移植正常肌肉中的水平。在正常的EDL肌肉中，无论是去神经支配、切断肌腱、去神经支配和血管离断，还是去神经支配、血管离断和切断肌腱后，PhK活性都会降低，但降低程度从未像同龄移植肌肉中那样大。在患有肌病的C57B1/10 mdx品系小鼠的胫前肌（TA）中，PhK活性也降低了，该品系小鼠的骨骼肌会持续发生退化和再生，同时保留其血管和神经连接。得出的结论是，移植肌肉中PhK活性的丧失是由于移植时发生的去神经支配、切断肌腱和再生等多种效应共同作用的结果。
