CHRONIC LEAD-EXPOSURE INDUCES ASTROGLIOSIS IN HIPPOCAMPUS AND CEREBELLUM

The aim of this study was to characterize the cytoskeletal intermediat e filaments, glial fibrillary acidic protein (GFAP), and vimentin in n ormal and lead treated rats, and to compare the astroglial response in the cerebellum and the hippocampus -two regions with great susceptibi lity to the toxic effects of lead. Experiments combined light and elec tron microscopy immunohistochemistry using antibodies to GFAP and to v imentin, and conventional transmission electron microscopy techniques. Chronic lead administration was provided through the drinking water ( 1g% lead acetate solution) and started when pups were 7 days old throu gh the mother's milk. Following weaning lead intoxicated offspring wer e continuously exposed during 9 months, and sacrificed, with their cor responding controls, by perfusion-fixation at 30, 60, 75, 90, 180 and 270 days of lead exposure. After 60 and 90 days of treatment, hypertro phic astrocytes were observed in the cerebellum and hippocampus. Addit ionally, in the same time-period more GFAP immunolabelled astrocytes w ere detected in the cerebellum but not in the hippocampus. These quali tative observations were confirmed by computerized image analysis quan tification. This effect was transient, even though the lead treatment was prolonged for 9 months and the blood-lead levels remained high aft er 30 days of the lead-exposure. After 90 days of lead administration, hypertrophic astrocytes started to decline and a gradual increment in the number of dense bodies, lipofuscin-like, was evidenced in astrocy tes, neurons, pericytes and microglial cells. The data suggest that ch ronic lead exposure induces an astrocytic reaction as a result of a di rect action of lead on astroglial cells or as a response to underlying neural damage. (C) 1994 Intox Press, Inc.