营养不良小鼠的神经肌肉传递

Neuromuscular transmission in dystrophic mice.

Carbonetto S

J Neurophysiol. 1977 Jul;40(4):836-43. doi: 10.1152/jn.1977.40.4.836.

Abstract

Neuromuscular transmission was studied in the extensor digitorum-longus muscle of dystrophic mice (strain 129/ReJ) by means of intracellular recording techniques. 2. In a large population of normal and dystrophic muscle fibers tested, the incidence of transmission failure was about 2% and showed no significant difference between the two groups. 3. Quantal size and quantum content of dystrophic junctions were found to be normal. This was true even of nerve terminal on apparently atrophied muscle fibers. 4. The facilitation ratio at dystrophic junctions was not significantly different from normal. 5. Dystrophic neuromuscular junctions exhibited an abnormality high frequency of giant spontaneous potentials. Application of tetrodotoxin (10(-6) M) and curare (10(-6) M) indicated that these potentials were caused by impulse-independent release of acetylcholine. 6. Neuromuscular transmission in dystrophic mice was found functionally normal and unrelated to the degenerative state of the muscle.

摘要

采用细胞内记录技术，对营养不良小鼠（129/ReJ品系）的趾长伸肌神经肌肉传递进行了研究。2. 在大量测试的正常和营养不良肌纤维中，传递失败的发生率约为2%，两组之间无显著差异。3. 发现营养不良性接头的量子大小和量子含量正常。即使是在明显萎缩的肌纤维上的神经末梢也是如此。4. 营养不良性接头处的易化率与正常情况无显著差异。5. 营养不良性神经肌肉接头处巨大自发电位的频率异常高。应用河豚毒素（10⁻⁶M）和箭毒（10⁻⁶M）表明，这些电位是由乙酰胆碱的非冲动依赖性释放引起的。6. 发现营养不良小鼠的神经肌肉传递在功能上是正常的，且与肌肉的退化状态无关。