Mutsaers S E, Carroll W M
Department of Pathology, Queen Elizabeth II Medical Centre, Nedlands, WA, Australia.
Acta Neuropathol. 1998 Aug;96(2):139-43. doi: 10.1007/s004010050873.
Mitochondrial accumulation has been reported at sites of degenerating nerve fibres. The reason for focal accumulation of mitochondria within axons has not previously been investigated. The aim of this study was to quantitate changes in mitochondrial concentration within demyelinated axons and determine if these changes were due to obstruction of the free passage of organelles within the fibre. The average number of mitochondria per unit area of axon within axons of normal cat optic nerve and optic nerve in which demyelination had been induced with anti-galactocerebroside (GC) was determined using transmission electron microscopy. Increased numbers of mitochondria were demonstrated at the site of demyelination, peaking at approximately two and a half times the value for normal non-lesioned nerves at 6-7 days after anti-GC administration [0.66+/-0.06 (SD) mitochondria per microm2 of axon compared to 0.28+/-0.04 in controls; P < 0.05]. The mitochondrial concentration gradually decreased over the next 20 days towards normal values. The concentration of mitochondria within non-myelinated axons of cat retina (0.55+/-0.18) was also determined and shown to be comparable to the values for the demyelinated optic axons (0.66+/-0.06). It is proposed that the accumulation of mitochondria within demyelinated axons reflects the adaptive process of the axon during the early restoration of impulse conduction rather than the obstruction of the free passage of organelles within the fibre.
据报道,在神经纤维退变部位有线粒体聚集。此前尚未研究轴突内线粒体局灶性聚集的原因。本研究的目的是定量脱髓鞘轴突内线粒体浓度的变化,并确定这些变化是否是由于细胞器在纤维内自由通行受阻所致。使用透射电子显微镜测定正常猫视神经轴突以及用抗半乳糖脑苷脂(GC)诱导脱髓鞘的视神经轴突每单位面积内线粒体的平均数量。结果显示,脱髓鞘部位的线粒体数量增加,在给予抗GC后6 - 7天达到峰值,约为正常未损伤神经的2.5倍[轴突每平方微米有0.66±0.06(标准差)个线粒体,而对照组为0.28±0.04;P < 0.05]。在接下来的20天里,线粒体浓度逐渐下降至正常值。还测定了猫视网膜无髓鞘轴突内的线粒体浓度(0.55±0.18),结果显示与脱髓鞘视神经轴突的值(0.66±0.06)相当。有人提出,脱髓鞘轴突内线粒体的聚集反映了轴突在冲动传导早期恢复过程中的适应性过程,而非细胞器在纤维内自由通行受阻。