Early post-natal, low-level lead exposure increases the number of PSA-NCAM expressing cells in the dentate gyrus of adult rat hippocampus

Although lead is widely known as a potent neurotoxin, the effect of lead exposure on the expression of the polysialic acid linked neural cell adhesion molecule (PSA-NCAM) remains unclear. We exposed Wistar rat pups to 0.2% lead acetate from postnatal day (PND) 1 to PND 30. This exposure protocol res...

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Bibliographic Details
Published in:Neurotoxicology (Park Forest South) 2006, Vol.27 (1), p.39-43
Main Authors: Heidmets, Lenne-Triin, Zharkovsky, Tamara, Jurgenson, Monika, Jaako-Movits, Kulli, Zharkovsky, Alexander
Format: Article
Language:English
Subjects:
Administration, Oral
Animals
Animals, Newborn
Biomarkers - analysis
Cell Count
Dentate gyms
Dentate Gyrus - cytology
Dentate Gyrus - metabolism
Immunohistochemistry
Lead - blood
Lead - pharmacokinetics
Lead - toxicity
Neural Cell Adhesion Molecule L1 - biosynthesis
Neural Cell Adhesion Molecule L1 - metabolism
Neurons - metabolism
Post-natal lead exposure
PSA-NCAM expressing cells
Rats
Rats, Wistar
Sialic Acids - biosynthesis
Sialic Acids - metabolism
Time Factors
Tubulin - analysis
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Summary:Although lead is widely known as a potent neurotoxin, the effect of lead exposure on the expression of the polysialic acid linked neural cell adhesion molecule (PSA-NCAM) remains unclear. We exposed Wistar rat pups to 0.2% lead acetate from postnatal day (PND) 1 to PND 30. This exposure protocol resulted in pup blood lead levels, which increased to 29.3 ± 5.0 mg/dl on PND 15, and subsequently rose to 34.2 ± 5.8 mg/dl at weaning. Corresponding brain tissue lead levels were 456 ± 23 ng/g on PND 15 and 781 ± 87 ng/g on PND 30. Animals were sacrificed on PND 80, when the blood and brain lead concentrations did not differ from those of the control group. Lead exposure induced a significant increase in the total number of PSA-NCAM expressing cells, compared to the control group ( p < 0.01), and did not change the proportion of cells co-expressing PSA-NCAM with glial or neuronal markers (calbindin, TuJ1, GFAP). These results suggest that early post-natal lead exposure induces persistent changes in the number of PSA-NCAM expressing cells, which could be, at least, partly the basis of impairments in the learning and memory formation, which follows low-level lead exposure.
ISSN:0161-813X
1872-9711
DOI:10.1016/j.neuro.2005.05.015