Early electrical field stimulation prevents the loss of spinal cord anterior horn motoneurons and muscle atrophy following spinal cord injury

Our previous study revealed that early application of electrical field stimulation（EFS） with the anode at the lesion and the cathode distal to the lesion reduced injury potential, inhibited secondary injury and was neuroprotective in the dorsal corticospinal tract after spinal cord injury（SCI）. The objective of this study was to further evaluate the effect of EFS on protection of anterior horn motoneurons and their target musculature after SCI and its mechanism. Rats were randomized into three equal groups. The EFS group received EFS for 30 minutes immediately after injury at T_（10）. SCI group rats were only subjected to SCI and sham group rats were only subjected to laminectomy. Luxol fast blue staining demonstrated that spinal cord tissue in the injury center was better protected; cross-sectional area and perimeter of injured tissue were significantly smaller in the EFS group than in the SCI group. Immunofluorescence and transmission electron microscopy showed that the number of spinal cord anterior horn motoneurons was greater and the number of abnormal neurons reduced in the EFS group compared with the SCI group. Wet weight and cross-sectional area of vastus lateralis muscles were smaller in the SCI group to in the sham group. However, EFS improved muscle atrophy and behavioral examination showed that EFS significantly increased the angle in the inclined plane test and Tarlov＇s motor grading score. The above results confirm that early EFS can effectively impede spinal cord anterior horn motoneuron loss, promote motor function recovery and reduce muscle atrophy in rats after SCI.

EFFECT OF 22kD,35kD PROTEIN MOLECULES FROM EXTRACT OF SKELETAL MUSCLE ON CULTURED ANTERIOR HORN MOTONEURON OF LUMBAR SPINE IN RAT

Ⅰ. INTRODUCTION The survival of motoneurons in vertebrates during their embryonic period depends on certain neurotrophic substances provided from their skeletal muscles. Skeletal muscles have been shown, in in vitro and in vivo experiments, to contain substances which are capable of enhancing the survival and development of motoneurons but preventing the

大鼠骨骼肌35kD运动神经诱向因子单克隆抗体的产生和鉴定

为探究脊髓运动神经元诱向因予,用大鼠腓骨肌提取液(PMe)作Phast电泳,分离PMe中能促进脊髓前角神经元生长的35kD蛋白带免疫动物。细胞融合,经MTT微量比色筛选,获得2株抗大鼠骨骼35kD蛋白的单克隆抗体。命名为ME10,MG9。2株单抗对体外培养的脊髓前角运动神经元的生长活性显示抑制作用,MTT OD值分别为0.023±0.003,0.030±0.005,以ME10抑制效应更强。与单独加35kD蛋白凝胶时促进细胞生长的OD值0.050±0.002比较,差别有显著意义(ME10 P<0.01,G9P<0.05)。为鉴定ME10单抗的特异性,进行中和试验。结果发现:ME10对运动神经元生长的抑制作用被35kD蛋白特异性地中和,说明ME10是3kD蛋白特异性抗体。用ME10单抗进行免疫组化反应,在骨骼肌细胞浆内,运动神经末稍都有免疫反应阳性物质,表明从腓肠肌组织提取液中分离的35kD蛋白是由骨骼肌细胞产生的神经诱向因子。

胚胎运动神经元移植对失神经肌肉影响的实验研究

目的 探讨胚胎运动神经元移植至入肌点前支配神经内对失神经肌肉萎缩的影响。 方法 取 2 0只健康 SD大鼠建立失神经腓肠肌动物模型 ,随机分移植组和对照组 (每组 10只 ) ;将胚胎14～ 18d的 SD鼠胚脊髓前角运动神经元的活细胞悬液注入移植组切断的胫神经远端 ,对照组注射等量的生理盐水。手术后第 3个月 ,进行腓肠肌肌力、肌湿重测定 ,组织和免疫化学检查以及胫神经纤维计数 ,并作图像分析。 结果 种植入胫神经内的鼠胚胎运动神经元能够存活。移植组腓肠肌肌力和肌湿重恢复率高于对照组 ,差异有显著性 (P<0 .0 1) ;肌纤维横截面积恢复率高于对照组 ,差异有显著性(P<0 .0 5 ) ,且 型、 型纤维面积均优于对照组 (P<0 .0 5 ) ;肌动蛋白的相对含量移植组高于对照组 ,差异有显著性 (P<0 .0 5 ) ;移植组运动终板结构清晰 ,而对照组大部分运动终板崩解 ,两组运动终板恢复率比较 ,差异有显著性 (P<0 .0 5 ) ;移植组神经纤维再生率为 0 .6 6 1± 0 .149,高于对照组的 0 .46 3±0 .10 9,差异有显著性 (P<0 .0 1)。 结论 胚胎运动神经元移植至外周神经内 ,便于靶组织获得神经营养 ,能延缓失神经肌肉的萎缩 。