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- af Bjerkén, Sara, et al.
(author)
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Inhibition of astrocytes promotes long-distance growing nerve fibers in ventral mesencephalic cultures
- 2008
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In: International Journal of Developmental Neuroscience. - : Wiley. - 0736-5748 .- 1873-474X. ; 26:7, s. 683-691
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Journal article (peer-reviewed)abstract
- Tyrosine hydroxylase-positive nerve fiber formation occurs in two diverse morphological patterns in rat fetal ventral mesencephalic slice cultures; one is non-glial-associated and the other is glial-associated. The aim of this study was to characterize the non-glial-associated nerve fibers and its relation to migration of astrocytes. Organotypic slice cultures were prepared from embryonic days 12, 14, and 18 rat fetuses and maintained for 5, 7 or 14 days in vitro. Inhibition of cell proliferation using cytosine beta-D-arabinofuranoside was conducted in embryonic day 14 ventral mesencephalic cultures. The treatment impaired astrocytic migration at 7 and 14 days in vitro. The reduced migration of astrocytes exerted a negative effect on the glial-associated tyrosine hydroxylase-positive nerve fibers, reducing the outgrowth from the tissue slice. The non-glial-associated outgrowth was, however, positively affected by reduced astrocytic migration, reaching distances around 3mm in 2 weeks, and remained for longer time in culture. Co-cultures of fetal ventral mesencephalon and frontal cortex revealed the cortex as a target for the non-glial-associated tyrosine hydroxylase-positive outgrowth. The age of the fetal tissue at plating affected the astrocytes such that older tissue increased the length of astrocyte migration. Younger tissue at plating promoted the presence of non-glial-associated outgrowth and long radial-glia-like processes, while older tissue promoted migration of neurons instead of formation of nerve fiber network. In conclusion, inhibition of astrocytic proliferation promotes the persistence of long-distance growing tyrosine hydroxylase-positive nerve fibers in ventral mesencephalic slices cultures. Furthermore, the long-distance growing nerve fibers target the frontal cortex and are absent in cultures derived from older tissue.
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| 3. |
- Miller, Marilyn T, et al.
(author)
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Autism associated with conditions characterized by developmental errors in early embryogenesis: a mini review.
- 2005
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In: International Journal of Developmental Neuroscience. - : Wiley. - 0736-5748 .- 1873-474X. ; 23:2-3, s. 201-219
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Journal article (peer-reviewed)abstract
- Autism is a complex developmental disorder without an established single etiology but with significant contributions from genetic studies, functional research, and neuropsychiatric and neuroradiologic investigations. The purpose of this paper is to review the findings in five studies involving individuals manifesting the characteristic findings of autism spectrum disorder associated with malformations and dysfunctions known to result from early embryogenic defects. These investigations include two associated with teratogens (thalidomide embryopathy, Mobius sequence with misoprostol) and three (most Mobius sequence cases, CHARGE association, Goldenhar syndrome) with no known etiology. These studies suggest that early embryonic development errors often involving cranial nerve palsies, internal and external ear malformations, ophthalmologic anomalies, and a variety of systemic malformations may be associated with autism spectrum disorders statistically more frequently than expected in a normal population. Although the exact time of developmental insult for each condition cannot be identified, the evidence is that it may occur as early as week 4 to 6+ of embryogenesis.
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| 7. |
- Viberg, Henrik
(author)
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Neonatal ontogeny and neurotoxic effect of decabrominated diphenyl ether (PBDE 209) on levels of synaptophysin and tau
- 2009
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In: International Journal of Developmental Neuroscience. - : Wiley. - 0736-5748 .- 1873-474X. ; 27:5, s. 423-429
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Journal article (peer-reviewed)abstract
- Mice and rats have a period of rapid growth and development that occurs postnatally, while in humans the corresponding period is perinatal. This gives us the opportunity to study direct effects of chemicals during developmental processes of the central nervous system (CNS) in murine animals. Mammals have a marked period of rapid brain growth and development, the brain growth spurt (BGS), which is postnatal in mice and rats, spanning the first 3-4 weeks of life and reaching its peak around postnatal day 10. The proteins synaptophysin and tau are involved in developmental processes in the nervous system during the BGS in mice. One class of flame retardants, polybrominated diphenyl ethers (PBDEs), is present and increasing in the environment and in human milk, which is also true for the only congener still in use, decabrominated diphenyl ether (2,2',3,3',4,4',5,5',6,6'-decaBDE, PBDE 209). The present study was divided into two parts (a) the neonatal ontogeny of synaptophysin and tau and (b) the developmental neurotoxic effect of PBDE 209 on synaptophysin and tau during the neonatal ontogeny in mice. The level of synaptophysin measured on postnatal days 1, 3, 7, 10, 14, and 28, increased continuously during the neonatal period, while tau has a bell-shaped ontogeny curve that peaks between postnatal days 7 and 10. The effects of PBDE 209 on the developmental expression of synaptophysin and tau were examined in neonatal NMRI male mice, orally exposed on day 3 to 20.1mg PBDE 209/kg body weight. The animals were euthanized 7 days after exposure to PBDE 209 and levels of synaptophysin and tau were analyzed in the hippocampus and cerebral cortex. The protein analysis showed that synaptophysin had increased significantly in the hippocampus, but not in the cerebral cortex, in mice 7 days after exposure to PBDE 209. The analysis of protein levels showed no changes in tau in the hippocampus or cerebral cortex 7 days after exposure to PBDE 209 on postnatal day 3. A recent study shows that neonatal PBDE 209-exposure can affect levels of BDNF (brain-derived neurotrophic factor), CaMKII (Ca(2+)/calmodulin-dependent protein kinase II), and GAP-43 (growth associated protein 43), which are proteins that are important for normal brain development. The present study shows that PBDE 209 affects the level of synaptophysin in the developing brain, which further supports the recent findings that PBDE 209 can disturb components of normal brain maturation and act as a developmental neurotoxicological agent. Furthermore, this suggests that certain proteins involved in developmental processes can serve as markers of developmental neurotoxicity.
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