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Age-related fragmentation of the motor endplate is not associated with impaired neuromuscular transmission in the mouse diaphragm

机译:与年龄有关的运动终板破碎与小鼠diaphragm肌神经肌肉传递受损无关

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摘要

As mammals age, their neuromuscular junctions (NMJs) gradually change their form, acquiring an increasingly fragmented appearance consisting of numerous isolated regions of synaptic differentiation. It has been suggested that this remodelling is associated with impairment of neuromuscular transmission, and that this contributes to age-related muscle weakness in mammals, including humans. The underlying hypothesis, that increasing NMJ fragmentation is associated with impaired transmission, has never been directly tested. Here, by comparing the structure and function of individual NMJs, we show that neuromuscular transmission at the most highly fragmented NMJs in the diaphragms of old (26–28 months) mice is, if anything, stronger than in middle-aged (12–14 months) mice. We suggest that NMJ fragmentation per se is not a reliable indicator of impaired neuromuscular transmission.
机译:随着哺乳动物的衰老,它们的神经肌肉接头(NMJ)逐渐改变其形式,获得越来越分散的外观,包括许多突触分化的孤立区域。已经提出,这种重塑与神经肌肉传递的损害有关,并且这导致了包括人在内的哺乳动物中与年龄有关的肌肉无力。 NMJ碎片增多与传播受损有关的基本假设从未得到直接检验。在这里,通过比较各个NMJ的结构和功能,我们发现,在年龄较大的(26-28个月)小鼠的fragment肌膜中,碎片最多的NMJ的神经肌肉传递要强于中年(12-14)个月)的老鼠。我们建议NMJ碎片本身不是神经肌肉传递受损的可靠指标。

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