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首页> 外文期刊>The Journal of Neuroscience: The Official Journal of the Society for Neuroscience >Damage-induced neuronal endopeptidase is critical for presynaptic formation of neuromuscular junctions.
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Damage-induced neuronal endopeptidase is critical for presynaptic formation of neuromuscular junctions.

机译：损伤诱导的神经内肽酶对于突触前神经肌肉连接的形成至关重要。

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摘要

Damage-induced neuronal endopeptidase (DINE) is a metalloprotease belonging to the neprilysin family. Expression of DINE mRNA is observed predominantly in subsets of neurons in the CNS and peripheral nervous system during embryonic development, as well as after axonal injury. However, the physiological function of DINE and its substrate remain unknown. We generated DINE-deficient mice to examine the physiological role of DINE. Shortly after birth, these mice died of respiratory failure resulting from a dysfunction of the diaphragm, which showed severe atrophy. As DINE was abundantly expressed in motor neurons and there was atrophy of the diaphragm, we analyzed the interaction between motor nerves and skeletal muscles in the DINE-deficient mice. Although there were no obvious deficiencies in numbers of motor neurons in the spinal cord or in the nerve trajectories from the spinal cord to the skeletal muscle in DINE-deficient mice, detailed histochemical analysis demonstrated a significant decrease of nerve terminal arborization in the diaphragm from embryonic day 12.5. In accordance with the decrease of final branching, the diaphragms from DINE-deficient mice exhibited only a few neuromuscular junctions. Similar changes in nerve terminal morphology were also apparent in other skeletal muscles, including the latissimus dorsi and the intercostal muscles. These data suggest that DINE is a crucial molecule in distal axonal arborization into muscle to establish neuromuscular junctions.
机译：损伤诱导的神经元内肽酶（DINE）是属于neprilysin家族的金属蛋白酶。 DINE mRNA的表达主要在胚胎发育期间以及轴突损伤后的中枢神经系统和周围神经系统的神经元亚群中观察到。但是，DINE及其底物的生理功能仍然未知。我们生成了DINE缺陷小鼠来检查DINE的生理作用。出生后不久，这些小鼠死于因a肌功能障碍而导致的呼吸衰竭，表现为严重的萎缩。由于DINE在运动神经元中大量表达并且存在the肌萎缩，因此我们分析了DINE缺陷小鼠中运动神经与骨骼肌之间的相互作用。尽管在DINE缺陷小鼠中脊髓或从脊髓到骨骼肌的神经轨迹中的运动神经元数量没有明显缺陷，但详细的组织化学分析表明，胚胎的the肌神经末梢的显着减少第12.5天。根据最终分支的减少，DINE缺陷小鼠的diaphragm肌仅表现出少数神经肌肉接头。神经末梢形态的类似变化在其他骨骼肌中也很明显，包括背阔肌和肋间肌。这些数据表明，DINE是远端轴突进入肌肉以建立神经肌肉连接的关键分子。

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