Vanadium compounds enhance adult neurogenesis after brain ischemia

Norifumi Shioda, Motohiro Morioka, Kohji Fukunaga

Research output: Contribution to journalReview articlepeer-review

4 Citations (Scopus)


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.

Original languageEnglish
Pages (from-to)413-417
Number of pages5
JournalYakugaku Zasshi
Issue number3
Publication statusPublished - 2008 Mar


  • Adult neurogenesis
  • Akt
  • Brain ischemia
  • Extracellular signal regulated kinase (ERK)
  • Vanadium compound

ASJC Scopus subject areas

  • Pharmacology
  • Pharmaceutical Science


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