PMID- 8584272
OWN - NLM
STAT- MEDLINE
DCOM- 19960318
LR  - 20131121
IS  - 0161-813X (Print)
IS  - 0161-813X (Linking)
VI  - 16
IP  - 3
DP  - 1995 Fall
TI  - Prolonged lead exposure modifies astrocyte cytoskeletal proteins in the rat 
      brain.
PG  - 389-401
AB  - The time-course and the regional astrocyte responses were studied during 15 
      months of continuous lead-exposure. Rat pups were exposed from postnatal day 1 
      (P1 group) and day 7 (P7 group) through the maternal milk, (1g% lead acetate 
      solution in the drinking water). Following weaning lead-exposed offspring were 
      treated during 15 months. Immunohistochemical staining for glial fibrillar acidic 
      protein (GFAP) and vimentin were used to evaluate astrocyte response. In 
      coincidence with previous results, after 2-3 months of treatment, we observed in 
      both groups a transient increase of GFAP immunoreactivity in hippocampal and 
      cerebellar astrocytes (first stage). After 4-12 months (second stage), the 
      hypertrophy 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 immunostaining of homologous sections 
      showed an increase of GFAP reactivity and the presence of vimentin + cells in the 
      upper and the lower limb, and in the hilus of the fascia dentata. GFAP and 
      vimentin astrocytic response extended to the adjacent cerebral cortex after 14 
      months. Although both cells showed a similar aspect, vimentin + cells showed a 
      smaller area and a restricted arrangement. However, in the cerebellum the 
      hypertrophy of vimentin positive astrocyte and Bergmann fibers was confined to 
      the white matter as observed in the first stage. Astrocyte alterations, the 
      recovery of vimentin expression and the appearance of lipofuscin-like bodies 
      induced by prolonged lead-exposure suggest modifications in neuronal 
      microenvironment, and might accelerate age-dependent changes in CNS.
FAU - Selvin-Testa, A
AU  - Selvin-Testa A
AD  - Instituto de Biologia Celular y Neurociencias, School of Medicine, University of 
      Buenos Aires, R. Argentina.
FAU - Loidl, C F
AU  - Loidl CF
FAU - Lopez, E M
AU  - Lopez EM
FAU - Capani, F
AU  - Capani F
FAU - Lopez-Costa, J J
AU  - Lopez-Costa JJ
FAU - Pecci-Saavedra, J
AU  - Pecci-Saavedra J
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
PL  - Netherlands
TA  - Neurotoxicology
JT  - Neurotoxicology
JID - 7905589
RN  - 0 (Proteins)
RN  - 2P299V784P (Lead)
SB  - IM
MH  - Analysis of Variance
MH  - Animals
MH  - Astrocytes/*drug effects
MH  - Brain Chemistry/*drug effects
MH  - Cerebellum/drug effects
MH  - Cytoskeleton/*drug effects
MH  - Female
MH  - Hippocampus/drug effects
MH  - Immunohistochemistry
MH  - Lead/*toxicity
MH  - Male
MH  - Proteins/*drug effects
MH  - Rats
MH  - Rats, Wistar
MH  - Time Factors
EDAT- 1995/01/01 00:00
MHDA- 1995/01/01 00:01
CRDT- 1995/01/01 00:00
PHST- 1995/01/01 00:00 [pubmed]
PHST- 1995/01/01 00:01 [medline]
PHST- 1995/01/01 00:00 [entrez]
PST - ppublish
SO  - Neurotoxicology. 1995 Fall;16(3):389-401.