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   <subfield code="a">Disruptive neuronal development by acrylamide in the hippocampal dentate hilus after developmental exposure in rats</subfield>
   <subfield code="h">[Elektronische Daten]</subfield>
   <subfield code="c">[Bunichiro Ogawa, Takumi Ohishi, Liyun Wang, Miwa Takahashi, Eriko Taniai, Hitomi Hayashi, Kunitoshi Mitsumori, Makoto Shibutani]</subfield>
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   <subfield code="a">To examine whether developmental exposure to acrylamide (AA) impairs neuronal development, pregnant Sprague-Dawley rats were treated with AA at 0, 25, 50 or 100ppm in drinking water from gestational day 6 until weaning on postnatal day 21. Offspring were immunohistochemically examined at the end of exposure. We investigated the expression of Reelin (a molecule regulating neuronal migration and positioning) in the hilus of the hippocampal dentate gyrus. As a positive control for direct exposure, AA (50mg/kg body weight) was administered to pups by intraperitoneal injection 3times per week during the lactation period. As well as pups directly injected with AA, maternally exposed offspring decreased body weight at 100ppm; increased dose-dependently the number of Reelin-immunoreactive cells (from 25ppm AA) and glutamic acid decarboxylase 67-immunoreactive cells (from 50ppm AA), confirming an increase in γ-aminobutyric acid-ergic interneurons. We also noted decreased apoptosis in the neuroblast-producing subgranular zone of the dentate gyrus of maternally exposed pups at 100ppm, as well as in directly AA-injected pups. These results suggest that a compensatory regulatory mechanism exists to correct impaired neurogenesis and mismigration caused by maternal exposure to AA during neuronal development. The lowest-observed-adverse-effect level of AA was determined to be 25ppm (3.72mg/kg body weight/day).</subfield>
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   <subfield code="a">Springer-Verlag, 2010</subfield>
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   <subfield code="a">Acrylamide</subfield>
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   <subfield code="a">Developmental neurotoxicity</subfield>
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   <subfield code="a">Neuronal migration</subfield>
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   <subfield code="a">Neurogenesis</subfield>
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   <subfield code="a">Dentate gyrus</subfield>
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   <subfield code="a">GABAergic interneuron</subfield>
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   <subfield code="a">AA : Acrylamide</subfield>
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   <subfield code="a">CA1 : Cornu ammonis 1</subfield>
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   <subfield code="a">CA2 : Cornu ammonis 2</subfield>
   <subfield code="2">nationallicence</subfield>
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  <datafield tag="690" ind1=" " ind2="7">
   <subfield code="a">CA3 : Cornu ammonis 3</subfield>
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  <datafield tag="690" ind1=" " ind2="7">
   <subfield code="a">Calb-D-28K : Calbindin-D-28K</subfield>
   <subfield code="2">nationallicence</subfield>
  </datafield>
  <datafield tag="690" ind1=" " ind2="7">
   <subfield code="a">GABA : γ-aminobutyric acid</subfield>
   <subfield code="2">nationallicence</subfield>
  </datafield>
  <datafield tag="690" ind1=" " ind2="7">
   <subfield code="a">GAD67 : Glutamic acid decarboxylase 67</subfield>
   <subfield code="2">nationallicence</subfield>
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   <subfield code="a">GD : Gestational day</subfield>
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  <datafield tag="690" ind1=" " ind2="7">
   <subfield code="a">PCNA : Proliferating cell nuclear antigen</subfield>
   <subfield code="2">nationallicence</subfield>
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   <subfield code="a">PND : Postnatal day</subfield>
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   <subfield code="a">Ogawa</subfield>
   <subfield code="D">Bunichiro</subfield>
   <subfield code="u">Laboratory of Veterinary Pathology, Tokyo University of Agriculture and Technology, 3-5-8 Saiwai-cho, Fuchu-shi, 183-8509, Tokyo, Japan</subfield>
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   <subfield code="a">Ohishi</subfield>
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   <subfield code="a">Wang</subfield>
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   <subfield code="u">Laboratory of Veterinary Pathology, Tokyo University of Agriculture and Technology, 3-5-8 Saiwai-cho, Fuchu-shi, 183-8509, Tokyo, Japan</subfield>
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   <subfield code="a">Takahashi</subfield>
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   <subfield code="u">Division of Pathology, National Institute of Health Sciences, 1-18-1 Kamiyoga, Setagaya-ku, 158-8501, Tokyo, Japan</subfield>
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   <subfield code="a">Taniai</subfield>
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   <subfield code="a">Hayashi</subfield>
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   <subfield code="a">Mitsumori</subfield>
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