Fujisawa K
Department of Neuropathology, Tokyo Metropolitan Institute for Neurosciences, Japan.
Acta Neuropathol. 1988;76(2):115-27. doi: 10.1007/BF00688095.
Axonal dystrophy in normal ageing can be studied in experimental animals. Primary sensory neurones show two different kinds of change with ageing, i.e. axonal dystrophy and axonal atrophy (degeneration). This paper reports the chronology and topography of these two processes in relation to growth and involution of these neurones throughout the lifespan of the rats used in this study. Axonal spheroids preferentially form at presynaptic terminal regions in many of the collaterals of central branches of the axons, i.e. in the posterior funiculus nuclei, posterior column and posterior funiculus. Axonal dystrophy in normal ageing is essentially a morbid process restricted to the terminal parts of the axon. It shows little tendency to expand retrogradely along the axon. Evidence is presented that spheroids in posterior funiculus also derive from terminal axons. Preference is also noted in the lumbosacral rather than cervical neurons, and in longer (posterior funiculus nuclei) rather than shorter (posterior column) collaterals. Quantitative study of myelinated fibres in posterior funiculus shows that they increase in number until middle age (400 days) of the animals, before beginning to decline. On the other hand, axonal atrophy begins to appear early in small numbers, and increases in numbers with age. Atrophy involves the whole length of the axon within the posterior funiculus from the start, suggesting, therefore, that it does not belong to a dying-back process. It is noteworthy that the main development of axonal dystrophy lies in the earlier half of the animals' life, while that of axonal atrophy lies in the latter half. This fact adds to the evidence that axonal dystrophy, as far as in normal ageing is concerned, is more related to the positive side of neuronal activity, e.g. one form of growth abnormality of axon.
正常衰老过程中的轴索性营养不良可在实验动物中进行研究。初级感觉神经元随衰老呈现两种不同的变化,即轴索性营养不良和轴索萎缩(退变)。本文报道了在本研究中所使用大鼠的整个生命周期内,这两个过程与这些神经元生长和退化相关的时间顺序和分布情况。轴突球状体优先在轴突中央支的许多侧支的突触前终末区域形成,即在薄束核、后索和薄束中。正常衰老中的轴索性营养不良本质上是一个局限于轴突终末部分的病态过程。它几乎没有沿轴突逆行扩展的趋势。有证据表明薄束中的球状体也源自轴突终末。还注意到腰骶部神经元而非颈部神经元、以及较长(薄束核)而非较短(后索)侧支存在偏好。对薄束中有髓纤维的定量研究表明,在动物中年期(400天)之前其数量增加,之后开始减少。另一方面,轴索萎缩在早期少量出现,并随年龄增加而增多。萎缩从一开始就累及薄束内轴突的全长,因此表明它不属于回返性退变过程。值得注意的是,轴索性营养不良的主要发展发生在动物生命的前半期,而轴索萎缩的主要发展发生在生命的后半期。这一事实进一步证明,就正常衰老而言,轴索性营养不良与神经元活动的积极方面关系更大,例如轴突生长异常的一种形式。