摘要
本文报道用辣根过氧化物酶 ( HRP)酶标生化方法探讨神经原性因素对小鼠比目鱼肌胞吞作用的影响及其与肌萎缩的关系。坐骨神经鞘内注射秋水仙素诱发比目鱼肌去神经样改变 ,再用脑提取液处理秋水仙素小鼠比目鱼肌 ;用河豚毒素 ( TTX)毛细管埋藏坐骨神经鞘内 ;另将变性神经提取液注入正常及人工冬眠小鼠的比目鱼肌间隙。测定比目鱼肌 HRP摄取的相对含量及肌肉湿重和总蛋白量。结果表明 ,脑提取液可完全消除秋水仙素引起的胞吞摄取增加和肌肉湿重及总蛋白量的减少。河豚毒素比秋水仙素对肌肉的去神经样影响要小 ,变性神经提取液对正常及人工冬眠小鼠的肌肉胞吞摄取明显增强 ,但肌肉湿重及总蛋白量无显著改变 ,提示在生理情况下 ,脑源性神经营养性生物大分子是维持肌肉胞吞稳态的首要因素 ,正常神经支配的肌肉 ,变性神经产物显著诱导胞吞增强 。
The effects of neurogenic factor on endocytosis of mouse soleus muscles(SM) and the relations with muscle atrophy were approached with the enzyme-labeled biochemical method-horseradish peroxidase(HRP). Colchicine was intrathecally injected into sciatic nerve to induce the denervation-like changes in SM and the brain extract(BE) was employed to treat SM treated with colchicine. Then, Tetrodotoxin(TTX) capillary tube was burried into the sheath of sciatic nerve. After that, the extract from degenerative nerve was injected into the soleus muscle of the normal and artificially-hibernated mouse. The relative content of HRP, the wet weight and the total protein amount of SM were determined. It was found that the brain extract can completely neutralize the increase of endocytosis and the decrease of the wet weight as well as the total amount of protein caused by colchicine. Compared with colchicine, TTX has less effect on denervation-like changes of SM. Degenerative nerve extract markedly increased the endocytosis of the normal and artificially-hibernated mouse muscles but the wet weight and the total amount of protein were not significantly modified. The results suggest that neurotrophic agent is a prime factor in maintaining the hoemostasis of muscle endocytosis whereas the muscles dominated by normal nerves, and the nerve degenerative products can promote the increase of endocytosis but can not give rise to muscle atrophy.
出处
《神经解剖学杂志》
CAS
CSCD
北大核心
2004年第3期305-308,共4页
Chinese Journal of Neuroanatomy
关键词
胞吞作用
肌萎缩
神经营养性因子
神经变性产物
突触传递
小鼠
比目鱼肌
endocytosis, muscle atrophy, neurotrophic agent, nerve degenerative product, axonal transport, synaptic trasmission