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Exposure to polybrominated diphenyl ethers 203 and 206 during the neonatal brain growth spurt affects proteins important for normal neurodevelopment in mice
Uppsala University, Disciplinary Domain of Science and Technology, Biology, Department of Physiology and Developmental Biology, Environmental Toxicology.
2009 (English)In: Toxicological Sciences, ISSN 1096-6080, E-ISSN 1096-0929, Vol. 109, no 2, 306-311 p.Article in journal (Refereed) Published
Abstract [en]

The period of rapid brain growth and development (BGS) is postnatal in mice and rats, spanning the first 3-4 weeks of life, reaching its peak around postnatal day 10, whereas in humans, the BGS is perinatal. CaMKII, GAP-43, synaptophysin, and tau play important roles during the BGS. One class of flame retardants, polybrominated diphenyl ethers (PBDEs), is present and increasing in the environment and in human milk. The only congener still in use, decabrominated diphenyl ether (PBDE 209), is thought to be debrominated into lower brominated congeners. In the present study, nona- and octabrominated PBDEs were examined. Neonatal mice were exposed to 21 mumol PBDE 203 or 206/kg bodyweight on postnatal day 10, and different brain regions were analyzed for CaMKII, GAP-43, synaptophysin, and tau, 24 h after exposure. The protein analysis showed that CaMKII and synaptophysin increased significantly in the hippocampus, but not in the cerebral cortex, after neonatal exposure to PBDE 203 or 206. Furthermore, there were no significant changes in the levels of GAP-43 and tau in the cerebral cortex or hippocampus after neonatal exposure to PBDE 203 or 206. This shows that PBDE 203 and 206 affect important proteins involved in normal maturation of the brain and strengthens our findings that highly brominated PBDEs cause developmental neurotoxicity. In addition, the increases in CaMKII and synaptophysin are the same changes seen after neonatal PBDE 209 exposure; supporting the suggestion that PBDE 209 must be metabolized, likely debrominated into lower brominated PBDEs, to exert its neurotoxic effects.

Place, publisher, year, edition, pages
2009. Vol. 109, no 2, 306-311 p.
Keyword [en]
PBDE 209, neurotoxicity, CaMKI, GAP-43, synaptophysin, tau
National Category
Biological Sciences
URN: urn:nbn:se:uu:diva-108057DOI: 10.1093/toxsci/kfp074ISI: 000266357900015PubMedID: 19380496OAI: oai:DiVA.org:uu-108057DiVA: diva2:234069
Available from: 2009-09-04 Created: 2009-09-04 Last updated: 2010-07-27Bibliographically approved

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