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“Polybrominated diphenyl ethers (PBDEs) are widely used commercial flame retardants that are accumulating in the environment. PBDEs may interfere with the development of key biological

systems, thus leaving children vulnerable to functional impairments in adulthood. There is a growing literature of animal studies that show subtle changes in motor and cognitive function following acute or repeated perinatal exposure to PBDEs. 2,2′,4,4′-Brominated diphenyl ether (BDE 47), a very stable PBDE congener, has been shown to accumulate in humans, perhaps as a breakdown product of other PBDEs. The current study examined developmental milestones in male C57BL/6 mice exposed to a single oral dose of BDE 47 (0, 1, 10, or 30 mg/kg) on postnatal day (PND) 10. Behavioral endpoints assessing sensory and motor maturation were examined on PNDs 12, 14, 16, 18, 32, and 88. Motor activity was also examined at 2 and 4 months in AZ 628 order PU-H71 ic50 a separate group of mice. BDE 47 exposure (particularly the highest dose) significantly increased body weight on PND 47 and thereafter. There was altered ontogeny in a few measures of neuromotor development; however, other developmental milestones and sensory responses

were not altered. Motor activity was altered at both 2 and 4 months, with BDE 47-treated mice (all dose groups) displaying pronounced hyperactivity at 4 months. These data indicate that acute exposure to BDE 47 during postnatal development may produce subtle changes in the development of neuromotor systems that may alter adult behavior. Published by Elsevier Inc.”
“Metallothioneins are central for the metabolism and detoxification of transition

metals. Exposure to mercury during early neurodevelopment is associated with neurocognitive impairment. Given the importance of metal lothioneins in mercury detoxification, metallothioneins may be a protective factor against mercury-induced neurocognitive impairment. Deletion of the murine metallothionein-1 and metallothionein-2 genes causes choice accuracy PS-341 cost impairments in the 8-arm radial maze. We hypothesize that deletions of metal lothioneins genes will make metallothionein-null mice more vulnerable to mercury-induced cognitive impairment. We tested this hypothesis by exposing MTI/MT2-null and wild-type mice to developmental mercury (HgC12) and evaluated the resultant effects on cognitive performance on the 8-arm radial maze. During the early phase of leaming metallothionein-null mice were more susceptible to mercury-induced impairment compared to wildtype mice. Neurochemical analysis of the frontal cortex revealed that serotonin levels were higher in metallothionein-null mice compared to wild-type mice. This effect was independent of mercury exposure. However, dopamine levels in mercury-exposed metallothionein-null mice were lower compared to mercury-exposed wildtype mice.