Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: EC:2.7.11.17 (CaMKII)
 4,029 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Mammals have a marked period of rapid brain growth and development (BGS), which is postnatal in mice and rats, spanning the first 3-4 weeks of life and reaching its peak around postnatal day 10. CaMKII, GAP-43 and BDNF play important roles during the BGS in mammals. One class of flame retardants, polybrominated diphenyl ethers (PBDEs), are present and increasing in the environment and in human milk, which is also true for the only congener still in use, decabrominated diphenyl ether (PBDE 209). In the present study, the brains from 1, 3, 7, 10, 14 and 28 days old mice, were analysed for CaMKII and GAP-43. The level of CaMKII increases continuously during the neonatal period, while GAP-43 has a bell-shaped ontogeny curve, which peaks around postnatal day 10, in mouse brain. Furthermore, the effects of PBDE 209 on the developmental expression of CaMKII, GAP-43 and BDNF were examined in mice. Neonatal NMRI-male mice were orally exposed on days 3-20.1mgPBDE 209/kg body weight. The animals were euthanized 7 days after exposure to PBDE 209 and levels of CaMKII, GAP-43 and BDNF were analysed in different brain regions. The protein analysis showed that CaMKII increased significantly in hippocampus, but not in cortex, in animals 7 days after exposure to PBDE 209. GAP-43 showed a significant increase in hippocampus and a significant decrease in cortex of animals 7 days after exposure to PBDE 209. BDNF decreased significantly in hippocampus, but not in cortex, in mice 7 days after exposure to PBDE 209. This shows that PBDE 209 affects important proteins involved in normal maturation of the brain and further strengthen our findings concerning PBDE 209 as a developmental neurotoxicological agent.
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PMID:Neonatal exposure to decabrominated diphenyl ether (PBDE 209) results in changes in BDNF, CaMKII and GAP-43, biochemical substrates of neuronal survival, growth, and synaptogenesis. 1806 78

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.
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PMID:Exposure to polybrominated diphenyl ethers 203 and 206 during the neonatal brain growth spurt affects proteins important for normal neurodevelopment in mice. 1938 Apr 96