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

• 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
• ISSN: 0161-813X; 1872-9711
• DOI: 10.1016/j.neuro.2005.05.015

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.