Vanadium Compounds Enhance Adult Neurogenesis after Brain Ischemia

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  • SHIODA Norifumi
    Department of Pharmacology, Graduate School of Pharmaceutical Sciences, Tohoku University
  • MORIOKA Motohiro
    Department of Neurosurgery, School of Medicine, Kumamoto University
  • FUKUNAGA Kohji
    Department of Pharmacology, Graduate School of Pharmaceutical Sciences, Tohoku University Tohoku University 21st Century COE Program “CRESCENDO,”

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  • 脳虚血におけるバナジウム化合物の神経新生亢進作用
  • ノウキョケツ ニ オケル バナジウム カゴウブツ ノ シンケイ シンセイ コウシン サヨウ

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Abstract

  Generation of neural precursors persists throughout life in the forebrain subventricular zone (SVZ) and dentate gyrus (DG) subgranular zone (SGZ) in rodent and human brains. In addition, newborn granule cells in the hippocampal DG are important for learning and memory formation. Brain injuries such as seizures or trauma could trigger endogenous programs for adult neurogenesis. Although brain ischemia also increases proliferation of neural progenitor cells in SVZ and SGZ, most neural progenitor cells are dead within 2 weeks after brain ischemia. In addition, there is no therapeutic agent to promote neurogenesis in the adult brain following brain injury. Here we found that intraperitoneal administrations of vanadium compounds, a stimulator of phosphatidylinositol 3-kinase (PI3K)/Akt and extracellular signal regulated kinase (ERK) pathways markedly enhances brain ischemia-induced neurogenesis. Thus, vanadium compounds are potential therapeutic agent to enhance ischemia-induced neurogenesis through PI3K/Akt and ERK activation.<br>

Journal

  • YAKUGAKU ZASSHI

    YAKUGAKU ZASSHI 128 (3), 413-417, 2008-03-01

    The Pharmaceutical Society of Japan

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