PROLONGED LEAD-EXPOSURE MODIFIES ASTROCYTE CYTOSKELETAL PROTEINS IN THE RAT-BRAIN

Citation
A. Selvintesta et al., PROLONGED LEAD-EXPOSURE MODIFIES ASTROCYTE CYTOSKELETAL PROTEINS IN THE RAT-BRAIN, Neurotoxicology, 16(3), 1995, pp. 389-401
Citations number
42
Categorie Soggetti
Pharmacology & Pharmacy",Neurosciences
Journal title
ISSN journal
0161813X
Volume
16
Issue
3
Year of publication
1995
Pages
389 - 401
Database
ISI
SICI code
0161-813X(1995)16:3<389:PLMACP>2.0.ZU;2-T
Abstract
The time-course and the regional astrocyte responses were studied duri ng 15 months of continuous lead-exposure. Rat pups were exposed from p ostnatal day 1 (P1 group) and day 7 (P7 group) through the maternal mi lk, (1g% lead acetate solution in the drinking water). Following weani ng lead-exposed offspring were treated during 15 months. Immunohistoch emical staining for glial fibrillar acidic protein (GFAP) and vimentin were used to evaluate astrocyte response. In coincidence with previou s results, after 2-3 months of treatment, we observed in both groups a transient increase of GFAP immunoreactivity in hippocampal and cerebe llar astrocytes (first stage). After 4-12 months (second stage), the h ypertrophy declined to near control levels despite the persistence of high-blood lead-levels; meanwhile, lipofuscin-like bodies appeared in neuronal and glial cells. After one year of treatment, the immunostain ing of homologous sections showed an increase of GFAP reactivity and t he presence of vimentin+ cells in the upper and the lower limb, and in the hilus of the fascia dentata. GFAP and vimentin astrocytic respons e extended to the adjacent cerebral cortex after 14 months. Although b oth cells showed a similar aspect, vimentin+ cells showed a smaller ar ea and a restricted arrangement. However, in the cerebellum the hypert rophy of vimentin positive astrocyte and Bergmann fibers was confined to the white matter as observed in the first stage. Astrocyte alterati ons, the recovery of vimentin expression and the appearance of lipofus cin-like bodies induced by prolonged lead-exposure suggest modificatio ns in neuronal microenvironment, and might accelerate age-dependent ch anges in CNS. (C) 1995 Intox Press, Inc.