[Vanadium compounds enhance adult neurogenesis after brain ischemia].
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.
Shioda
Norifumi
N
Department of Pharmacology, Graduate School of Pharmaceutical Sciences, Tohoku University, Sendai, Japan.
Morioka
Motohiro
M
Fukunaga
Kohji
K
D000818:Animals; D001921:Brain / Q000502:physiology*; D002545:Brain Ischemia / Q000188:drug therapy* / Q000503:physiopathology*; D048049:Extracellular Signal-Regulated MAP Kinases / Q000378:metabolism; D006801:Humans; D007274:Injections, Intraperitoneal; D009416:Nerve Regeneration; D009474:Neurons / Q000502:physiology*; D019869:Phosphatidylinositol 3-Kinases / Q000378:metabolism; D013268:Stimulation, Chemical; D017968:Vanadium Compounds / Q000008:administration & dosage / Q000494:pharmacology / Q000627:therapeutic use*
D017968:Vanadium Compounds; D019869:Phosphatidylinositol 3-Kinases; D048049:Extracellular Signal-Regulated MAP Kinases