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Neontatal exposure to deca-brominated diphenyl ether (PBDE 209) causes dose-response changes in spontaneous behaviour and cholinergic susceptibility in adult mice
Uppsala University, Disciplinary Domain of Science and Technology, Biology, Department of Physiology and Developmental Biology, Environmental Toxicology. (Per Eriksson)
Uppsala University, Disciplinary Domain of Science and Technology, Biology, Department of Physiology and Developmental Biology, Environmental Toxicology.
Uppsala University, Disciplinary Domain of Science and Technology, Biology, Department of Physiology and Developmental Biology, Environmental Toxicology.
Uppsala University, Disciplinary Domain of Science and Technology, Biology, Department of Physiology and Developmental Biology, Environmental Toxicology.
2008 (English)In: Neurotoxicology, ISSN 0161-813X, E-ISSN 1872-9711, Vol. 29, no 6, 911-919 p.Article in journal (Refereed) Published
Abstract [en]

Polybrominated diphenyl ethers (PBDEs), used as additive flame-retardants, are increasing in the environment and are present in human mother's milk, newborns and toddlers. We reported earlier that several PBDEs, highly brominated PBDEs, caused developmental neurotoxic effects in mice, manifested as persistent aberrations in spontaneous behaviour, habituation capability, learning and memory, and changes in the cholinergic system.The present study was undertaken to explore the dose–response effects of PBDE 209 on spontaneous behaviour, habituation and its effects on the murine cholinergic system. Neonatal male NMRI mice were given 1.4, 2.3, 14 or 21 μmol PBDE 209/kg body weight, when 3 days old. The agent was administered as a single oral dose via a metal gastric tube. Spontaneous behaviour and response to the cholinergic agonist nicotine were observed in adult mice at 2 and 4 months of age. Mice were also observed for anxiety-like behaviour in an elevated plus-maze. Adult mice, 2 and 4 months old, showed a dose–response related change in spontaneous behaviour, viz. were hyperactive and showed reduced or lack of habituation, effects that worsen with age. At the adult age of 4 months the susceptibility of the cholinergic system was also affected in a dose–response related manner, viz. reduced and/or hypoactive response to nicotine. This shows that PBDE 209 can be as potent as the lower brominated PBDEs in causing developmental neurotoxic defects.

Place, publisher, year, edition, pages
2008. Vol. 29, no 6, 911-919 p.
Keyword [en]
Deca-brominated diphenyl ether, Flame-retardant, Neonatal, Spontaneous behaviour, Cholinergic, PBDE 209
National Category
Pharmacology and Toxicology
Identifiers
URN: urn:nbn:se:uu:diva-99061DOI: 10.1016/j.neuro.2008.09.08ISI: 000261551800001OAI: oai:DiVA.org:uu-99061DiVA: diva2:202042
Available from: 2009-03-06 Created: 2009-03-06 Last updated: 2017-12-13Bibliographically approved
In thesis
1. Neonatal Exposure to Highly Brominated Diphenyl Ethers and Perfluorinated Compounds: Developmental Dependent Toxicity and Interaction
Open this publication in new window or tab >>Neonatal Exposure to Highly Brominated Diphenyl Ethers and Perfluorinated Compounds: Developmental Dependent Toxicity and Interaction
2009 (English)Doctoral thesis, comprehensive summary (Other academic)
Abstract [en]

This thesis investigated the developmental neurotoxic effects of neonatal exposure to highly brominated diphenyl ethers (PBDEs) and perfluorinated compounds (PFCs), alone or in combinations, during a critical period of the brains’ rapid growth and development, in mice. The compounds investigated were the decaBDE (PBDE 209), nonaBDE (PBDE 206), octaBDE (PBDE 203), heptaBDE (PBDE 183), and three PFCs, PFOS, PFOA, and PFDA.

PBDEs and PFCs have been identified as emerging classes of persistent environmental compounds, present in wildlife as well as humans, and present at higher levels in infants/children, compared to older persons. Individuals can be exposed to these compounds throughout her/his lifetime and newborn/children can be exposed to toxicants both via the mothers’ milk and directly via ingestion and inhalation.

The brain growth spurt (BGS) is defined by rapid growth and developmental of the brain. For rodents (mice and rats), the BGS is postnatal spanning the first 3-4 weeks after birth. In humans this period begins during the third trimester of pregnancy and continues throughout the first two years of life. It has been shown that several environmental toxicants can induce permanent disorders in brain function when administered to the neonatal mouse, during the BGS.

This thesis shows that highly brominated PBDEs, including PBDE 209, PBDE 206, and PBDE 203 can cause developmental neurotoxic effects, when given directly to the neonatal mouse. Of the investigated PFCs, PFOS and PFOA were shown to cause similar effects as the PBDEs. Furthermore, PBDE 209 and PFOA can at low doses interact and enhance the neurotoxic effects in mice. Effects in the adult animal included; deranged spontaneous behavior, reduced or lack of habituation, decreased learning and memory abilities, and increased susceptibility of the cholinergic system. Both classes of compounds were shown to affect proteins (CaMKII, GAP-43, synaptophysin, and tau) important for neuronal growth and synaptogenesis in the neonatal mouse brain.

Place, publisher, year, edition, pages
Uppsala: Acta Universitatis Upsaliensis, 2009. 67 p.
Series
Digital Comprehensive Summaries of Uppsala Dissertations from the Faculty of Science and Technology, ISSN 1651-6214 ; 619
National Category
Biological Sciences
Research subject
Ecotoxicology
Identifiers
urn:nbn:se:uu:diva-99255 (URN)978-91-554-7456-0 (ISBN)
Public defence
2009-04-24, Lindahlsalen, EBC, Norbyvägen 18A, Uppsala, 13:15 (English)
Opponent
Supervisors
Available from: 2009-04-02 Created: 2009-03-11 Last updated: 2009-09-04Bibliographically approved

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