DEVELOPMENTAL PROFILE OF NONHEME IRON DISTRIBUTION IN THE RAT-BRAIN DURING ONTOGENY

Authors
Citation
T. Moos, DEVELOPMENTAL PROFILE OF NONHEME IRON DISTRIBUTION IN THE RAT-BRAIN DURING ONTOGENY, Developmental brain research, 87(2), 1995, pp. 203-213
Citations number
32
Categorie Soggetti
Neurosciences
ISSN journal
01653806
Volume
87
Issue
2
Year of publication
1995
Pages
203 - 213
Database
ISI
SICI code
0165-3806(1995)87:2<203:DPONID>2.0.ZU;2-N
Abstract
The entry of iron from blood into the developing rat brain was studied by means of non-heme iron-histochemistry. The content of non-heme iro n in the endothelial cells was manifest already from E14, declined fro m P3 to P5, and was almost absent on P10-P15. The choroid plexus epith elial cells of either ventricle was non-heme iron-containing from E14. Non-heme iron-containing macrophages situated in the stroma of the ch oroid plexus were also observed from E14. From E19, the macrophage-lik e cells tended to invade into (a) regions with transitory structures l ike the intermediate zone of the cerebral hemisphere, (b) developing a xonal tracts like corpus callosum and internal capsule, and (c) deep l ayers of the tectum, a region with an extensive degree of naturally oc curring cell death. The amoeboid macrophage-like cells observed in the brain parenchyma gradually acquired prolonged extensions and apparent ly differentiated into ramified microglia-like cells, which later lost their non-heme iron-content. Thus, at P70, non-heme iron-positive mic roglia-like cells were hardly seen reflecting the transitory event of non-heme iron in microglia-like cells. At P200, non-heme iron-containi ng microglia cells and oligodendrocytes appeared in manifestly higher number than at P70, a phenomenon probably related to aging. These resu lts delineate for the first time the appearance of iron in the develop ing brain. The results are of relevance for understanding the potentia l of iron-deficiency for harming the developing central nervous system , generally by decreased transport of iron through brain capillaries a nd choroid plexus, and specifically by an impaired modulation of the d eveloping brain parenchyma by iron-containing macrophages.