Adult Neurogenesis Workshop Report

نویسندگان

  • Shira Rosenzweig
  • Paul Luu
چکیده

the use of SDF-1 and SCF provides promise in enhancing regeneration in aged neural stem cells. Dr. Masashi Fujitani, a postdoctoral fellow in Dr. F. D. Miller’s laboratory at the Department of Physiology, shared his recent findings in a presentation titled “TAp73 regulates the self-renewal and maintenance of CNS neural stem cells.” Dr. Fujitani researches the molecular basis behind the ability of neural precursor cells to self-renew, and has identified a specific gene, TAp73 (p53 tumor suppressor gene homolog), which plays an important role in this process. Neurosphere assay and immunohistological techniques demonstrated that in hippocampal cultures prepared from TAp73 knockout mice, the self-renewal and proliferation of neuronal precursor cells are reduced. In subsequent experiments TAp73 was knocked down in utero, resulting in a similar decrease in proliferation. Dr. Fujitani then demonstrated that TAp73 also plays a role in adult neurogenesis. When comparing hippocampal sections stained for BrdU and NeuN, he found a decrease in the number of double-stained cells in TAp73 knockout mice compared to control mice. Using microarray analysis Dr. Fujitani had successfully identified Hey2 promoter as a possible downstream target of TAp73. Dr. Tzong-Shiue Yu, a postdoctoral fellow in Dr. P. W. Frankland’s laboratory at the Department of Physiology, outlined his recent findings in a presentation titled “Neuronal Activity in Entorhinal Cortex Regulates Adult Neurogenesis”. Dr. Yu’s work examines whether exposure to enriched environment promotes neurogenesis by increasing the inputs relayed to the DG from the entorhinal cortex. Dr. Yu used viral transfection to transiently over-express either dominant-negative KCNQ2 or Kir 2.1 in the entorhinal cortex of rats (the primary input to the DG), thus increasing or decreasing the excitability in this region, respectively. Preliminary results suggested that increased excitability of the entorhinal cortex, which would increase the inputs into the DG (possibly in a similar way to Adult neurogenesis workshop report

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عنوان ژورنال:

دوره 4  شماره 

صفحات  -

تاریخ انتشار 2010