摘要
目的:观察周围神经损伤后降钙素基因相关肽(Calcitoningen-relatedpeptide,CGRP)在脊髓神经元及运动终板中的变化,以探讨CGRP与运动终板退行性变的关系。方法:以切断坐骨神经的大鼠为模型,以免疫组化方法结合计算机图像分析技术检测CGRP在脊髓神经元及运动终板中的变化,并以镀银法作同期运动终板退行性变的观察。结果:神经损伤1周后CGRP即在脊髓前角运动神经元中升至最高,并持续4周,8周后恢复正常。在正常胫前肌中可见神经末梢及运动终板均被CGRP抗体清晰标记。神经损伤1周后,CGRP在神经末梢和运动终板中即完全消失。神经切断后镀银法显示运动终板在前2周无明显变化,3周运动终板开始部分染色模糊、浅淡,8周运动终板完全消失。结论:在运动终板退行性变的机制中,CGRP的缺乏可能是一个重要的因素。
AIM:To discuss the relationship between calcitonin gene relative peptide(CGRP) and degeneration of motor end plates by observing the changes of CGRP in the spinal cord neurons and motor end plate after sciatic nerve injury. METHODS:Rat models were established by cutting sciatic nerve.Immunohistochemical technique with computer image analysis was used to detect the changes of CGRP in the spinal cord neurons and motor end plate,and in the corresponding period,the degeneration of motor end plate was observed by using silver impregnation method. RESULTS:One week after cutting the sciatic nerve,CGRP reached the topmost in the anterior horn motor neurons of spinal cord,and lasted 4 weeks,and then recovered to normal 8 weeks later.Antibody of CGRP was labeled clearly at the nerve terminals and motor end plate in the normal tibialis anterior muscle.After 1 week nerve injury,CGRP completely disappeared at the nerve terminal and motor end plate.No changes were observed within the first 2 weeks after cutting nerve at the motor end plate with deargentation,the staining of motor end plate became clouding and light from the third week,and the motor end plate completely disappeared in the eighth week. CONCLUSION:Lack of CGRP is maybe one of the important factors in the mechanisms of the motor end plate degeneration.
出处
《中国临床康复》
CAS
CSCD
2004年第20期4008-4009,i004,共3页
Chinese Journal of Clinical Rehabilitation
