title: Study of axonal dystrophy. III. Posterior funiculus and posterior column of ageing and old rats.
abstract: 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.
authors.affiliation: Department of Neuropathology, Tokyo Metropolitan Institute for Neurosciences, Japan.
authors.forename: K
authors.initials: K
authors.lastname: Fujisawa
mesh_terms: D000375:Aging / Q000473:pathology*; D000818:Animals; D001284:Atrophy; D001369:Axons / Q000502:physiology / Q000648:ultrastructure*; D002452:Cell Count; D008297:Male; D008854:Microscopy, Electron; D009410:Nerve Degeneration; D009413:Nerve Fibers, Myelinated / Q000502:physiology / Q000648:ultrastructure; D051381:Rats; D011919:Rats, Inbred Strains; D013116:Spinal Cord / Q000254:growth & development / Q000473:pathology*