Study of Axonal Dystrophy. Ii. Dystrophy and Atrophy of the Presynaptic Boutons: A Dual Pathology

Abstract

In succession to the previous quantitative work, a qualitative study has been carried out on the nature of a dual pathology affecting presynaptic boutons in the posterior tract nuclei of ageing rats. Based on the morphology of dystrophic boutons in early stage, it is concluded that the initial and therefore essential characteristic of dystrophic process is an abnormal increase of normal axonal components within the presynaptic boutons, and that various abnormal substructures of spheroids hitherto reported in the literature are probably the results of their secondary metamorphosis. The dystrophic process within the posterior tract nuclei is a selective one, involving presynaptic boutons and preterminal axons only of the posterior tract fibres. Comparison of the frequency of early dystrophic boutons and of fully grown-up spheroids indicates that a small percentage of boutons deriving from posterior tract fibres become dystrophic and of these dystrophic boutons only a small percentage again continue to develop unto large spheroids, throughout lifespan of the animals. On the other hand, in search of a morphological counterpart for the age-related decrease of volume ratio of presynaptic boutons to the neuropil, some dubious atrophic changes were also found in presynaptic boutons, which could have been easily missed from observation if studied qualitatively alone. Accordingly, no less numerous boutons other than dystrophic ones are supposed to atrophy 'independently' and to disappear 'silently' during the same period. The dystrophic and the atrophic changes involve different boutons (of different or the same terminal axons) within the same gray matter. This dual pathology of boutons needs further elucidation of its neurocytopathological as well as neurobiological background in the future.

Changes with Age in the Number and Size of Myelinated Axons in the Rat L₄ Dorsal Spinal Root

“…These changes consisted mainly of demyeli nation and were tentatively interpreted as a manifestation of pressure neuropathy, with a possible superimposed senile distal axonal degeneration at later stages . The finding in aged rats of distal axonal degeneration in the dorsal tail nerve, which is unlikely to be exposed to recurrent pressure [King and Thomas, 1982], com pares to the occurrence of dystrophic and atrophic terminal portions of central pro cesses of primary sensory neurons at the level of gracile and cuneate nuclei [Fujisawa and Shiraki, 1980], which also do not seem to represent a pressure neuropathy.…”

Biochemical Mechanisms Underlying Primary Degeneration of Axons

“…36 Distal axonal changes are especially pronounced in the gracile nucleus, where the central projection of primary sensory neurons accumulate large amounts of branched tubulovesicular profiles. 148 Similar changes are found in toxic states associated with p-bromophenylacetyl urea, diethyldithiocarbamate, and zinc pyridinethione and in metabolic disturbances in which intestinal malabsorption is a prominent feature. Further examples include experimental vitamin E deficiency 149 and the inherited neuroaxonal dystrophies of man 150 and dog.…”

Encephalomyelitis, brain tumors, neuromuscular diseases and miscellaneous disorders

“…Biological characteristics of astrocytes and their relationship to the blood–brain barrier have been ultrastructurally presented by Ikuta et al and Kawai et al 47,48 Morphological and developmental analysis of microglia have been continuously reported by Fujita and Kitamura, and Kitamura et al , 49,50 and the report using chimeric rats has provided an insight into the origin of microglia. 51 Ultrastructural studies on axonal dystrophy and aging neurons by Fujisawa, and Fujisawa and Shiraki, 52,53 histopathological studies of alobar holoprosencephaly by Mizuguchi and Morimatsu, 54,55 and a plethora of other investigations and studies have been reported that would be beyond our ability to introduce and describe in the present short report. They will be listed in the next anniversary edition.…”