Involvement of decreased glutamate receptor subunit GluR2 expression in lead-induced neuronal cell death

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Author(s)

Abstract

Lead is known to induce neurotoxicity, particularly in young children, and GluR2, an AMPA-type glutamate receptor subunit, plays an important role in neuronal cell survival. Therefore, we hypothesized that altered GluR2 expression plays a role in lead-induced neuronal cell death. To test this idea, we investigated the effect of exposure to 5 and 20 µM lead for 1-9 days on the viability and GluR2 expression of primary-cultured rat cortical neurons. The number of trypan-blue stained cells was increased by exposure to 5 µM lead for 9 days or 20 µM lead for 7-9 days, and LDH release was increased after exposure to 20 µM lead for 9 days. GluR2 expression was reduced by exposure to 5-100 µM lead, but not 0.1-1 µM lead, for 9 days. Immunocytochemistry also confirmed that GluR2 expression was decreased in the presence of lead. Application of 50 ng/ml brain-derived neurotrophic factor (BDNF) led to a recovery of lead-induced neuronal cell death, accompanied with increased GluR2 expression. Our results suggest that long-term exposure to lead induces neuronal cell death, in association with a decrease of GluR2 expression.

Journal

  • The Journal of Toxicological Sciences

    The Journal of Toxicological Sciences 38(3), 513-521, 2013-06-01

    The Japanese Society of Toxicology

References:  39

Codes

  • NII Article ID (NAID)
    10031158917
  • NII NACSIS-CAT ID (NCID)
    AN00002808
  • Text Lang
    ENG
  • Article Type
    ART
  • ISSN
    03881350
  • NDL Article ID
    024784162
  • NDL Call No.
    Z19-1022
  • Data Source
    CJP  NDL  J-STAGE 
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