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肌肉代偿性肥大后大鼠跖肌运动神经元的功能和结构变化

Functional and structural changes of rat plantaris motoneurons following compensatory hypertrophy of the muscle.

作者信息

Finkelstein D I, Lang J G, Luff A R

机构信息

Department of Physiology, Monash University, Clayton, Victoria, Australia.

出版信息

Anat Rec. 1991 Jan;229(1):129-37. doi: 10.1002/ar.1092290115.

DOI:10.1002/ar.1092290115
PMID:1996779
Abstract

The conduction velocity and histological structure of motoneurons innervating normal and hypertrophied rat plantaris muscles were investigated. Hypertrophy was produced by ablation of synergist muscles. Single motor units were obtained by ventral root dissection and conduction velocities measured. The structure of neurons was investigated following retrograde labeling with horseradish peroxidase. A combined silver, gold and cholinesterase staining method was developed to study the motor endplate. In addition, the peripheral nerve was fixed, embedded in Araldite, and sectioned for determination of axonal size and myelin thickness. Conduction velocity of motor axons decreased following hypertrophy of the skeletal muscle (control CV = 75.8 +/- 8.9 m s-1, n = 94, hypertrophy CV = 69.0 +/- 12.3 m s-1, n = 84). However, no alteration in the size of motor axons or myelin thickness could account for this alteration in conduction velocity. Mean motoneuronal soma size decreased following muscle hypertrophy (soma diameter: control 36.1 +/- 4.6 microns, n = 283, hypertrophy 32.9 +/- 4.5 microns, n = 294). The complexity of the motor endplate increased following hypertrophy with an increased occurrence of nodal sprouts. In addition, the area of cholinesterase staining increased following hypertrophy (control 588.1 +/- 297.2 microns 2, n = 269, hypertrophy 857.7 +/- 357.0 microns 2, n = 269). This study found that both the morphological and physiological parameters of motoneurons innervating a hypertrophied muscle were shifted toward those of normal rat slow motor units.

摘要

对支配正常和肥大大鼠跖肌的运动神经元的传导速度和组织学结构进行了研究。肥大是通过切除协同肌产生的。通过腹根解剖获得单个运动单位并测量传导速度。用辣根过氧化物酶逆行标记后研究神经元的结构。开发了一种银、金和胆碱酯酶联合染色方法来研究运动终板。此外,将外周神经固定、包埋在环氧树脂中并切片以测定轴突大小和髓鞘厚度。骨骼肌肥大后运动轴突的传导速度降低(对照组CV = 75.8±8.9 m/s,n = 94,肥大组CV = 69.0±12.3 m/s,n = 84)。然而,运动轴突大小或髓鞘厚度的改变无法解释传导速度的这种变化。肌肉肥大后运动神经元胞体平均大小减小(胞体直径:对照组36.1±4.6微米,n = 283,肥大组32.9±4.5微米,n = 294)。肥大后运动终板的复杂性增加,结旁芽的出现增加。此外,肥大后胆碱酯酶染色面积增加(对照组588.1±297.2平方微米,n = 269,肥大组857.7±357.0平方微米,n = 269)。本研究发现,支配肥大肌肉的运动神经元的形态学和生理学参数均向正常大鼠慢运动单位的参数转变。

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