Glycogenosomes in the aging rat brain: their occurrence in the visual pathways

Citation
Jb. Cavanagh et Hb. Jones, Glycogenosomes in the aging rat brain: their occurrence in the visual pathways, ACT NEUROP, 99(5), 2000, pp. 496-502
Citations number
36
Categorie Soggetti
Neurosciences & Behavoir
Journal title
ACTA NEUROPATHOLOGICA
ISSN journal
00016322 → ACNP
Volume
99
Issue
5
Year of publication
2000
Pages
496 - 502
Database
ISI
SICI code
0001-6322(200005)99:5<496:GITARB>2.0.ZU;2-8
Abstract
The significance of glycogenosomes (glycogen bodies), frequently seen in pe ripheral neurites of aging rats, is unknown and their occurrence elsewhere in nervous tissue is poorly documented. During the course of another study these bodies were observed by light microscopy in the visual pathways of ag ing rats where they have not previously been noted, and this report documen ts their occurrence, localisation and changes in density with age. Using th e periodic acid-Schiff stain, small brightly red-staining bodies, digested by diastase and containing beta-glycogen particles, were seen in increasing numbers in the neuropil of the superior colliculi in brain sections from a nimals of 5 months of age onwards. From 1 year until more than 2 years of a ge they steadily became more numerous in the outer one third of the superio r colliculus, but remained small, rarely exceeding 4 mu m. They were also f ound at later times in small numbers lying singly in the optic tract, the o ptic chiasm and optic nerves, although rarely in lateral geniculate nuclei. Similar bodies were also found to accumulate with age in the retinal photo receptor cell layer. Changes in their densities and size with age in both r egions have been documented and it is suggested that, while their occurrenc e in retinal photoreceptor cells may be due to sustained light damage leadi ng to mitochondrial oxidative stress. it is difficult to implicate this mec hanism for their occurrence in retino-tectal nerve fibres. The role of phys ical trauma, suggested for the presence of these bodies in aging peripheral axone, can be excluded and they appear not to be related to polyglucosan b odies.