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首页> 外文期刊>CNS neuroscience & therapeutics. >Sigma‐1 Receptor Knockout Impairs Neurogenesis in Dentate Gyrus of Adult Hippocampus iVia/i Down‐Regulation of NMDA Receptors
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Sigma‐1 Receptor Knockout Impairs Neurogenesis in Dentate Gyrus of Adult Hippocampus iVia/i Down‐Regulation of NMDA Receptors

机译：Sigma-1受体敲除损害成年海马 Via NMDA受体下调的齿状回神经元发生。

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Summary Aims This study investigated the influence of sigma‐1 receptor (σ1 R ) deficiency on adult neurogenesis. Methods We employed 8‐week‐old male σ1 R knockout (σ1 R ?/?) mice to examine the proliferation and differentiation of progenitor cells, and the survival and neurite growth of newborn neurons in hippocampal dentate gyrus ( DG ). Results In comparison with wild‐type ( WT ) littermates, the numbers of 24‐h‐old B rd U + cells and K i67+ cells in σ1 R ?/? mice increased, while the number of 28‐day‐old B rd U + cells decreased without changes in proportion of B rd U +/ N eu N + cells and B rd U +/ GFAP + cells. The neurite density of newborn neurons was slightly reduced in σ1 R ?/? mice. In DG granular cells, N ‐methyl‐ d ‐aspartate ( NMDA )‐activated current ( I NMDA ) and phosphorylation of NMDA receptor ( NMDA r) NR 2 B were reduced in σ1 R ?/? mice without the alteration of NR 2 B expression and membrane properties compared to WT mice. The NR 2 B antagonist abolished the difference in I NMDA between σ1 R ?/? mice and WT mice. The application of NMDA r agonist in σ1 R ?/? mice prevented the over‐proliferation of cells and reduction in newborn neurons, but it had no effects on the hypoplastic neurite. The administration of NMDA r antagonist in WT mice enhanced the cell proliferation and depressed the survival of newborn neurons. Conclusion The σ1 R deficiency impairs neurogenesis in DG through down‐regulation of NMDA rs.
机译：概述目的这项研究调查了sigma-1受体（σ1R）缺乏对成人神经发生的影响。方法我们采用8周龄的雄性σ1R基因敲除（σ1R？/？）小鼠检查祖细胞的增殖和分化，以及海马齿状回（DG）中新生神经元的存活和神经突生长。结果与野生型（WT）同窝仔相比，σ1R？/？中24 h Brd U +细胞和K i67 +细胞的数量。小鼠增加，而28天的Brd U +细胞数量减少，而Brd U + / N eu N +细胞和Brd U + / GFAP +细胞的比例没有变化。新生神经元的神经突密度以σ1R？/？降低。老鼠。在DG颗粒细胞中，σ1R？/？降低了N-甲基-d-天门冬氨酸（NMDA）激活电流（I NMDA）和NMDA受体（NMDA r）NR 2 B的磷酸化。与野生型小鼠相比，没有改变NR 2 B表达和膜特性的小鼠。 NR 2 B拮抗剂消除了σ1Rα/β之间的NMDA差异。小鼠和野生型小鼠。 NMDA激动剂在σ1R？/？中的应用。小鼠可预防细胞过度增殖和新生神经元减少，但对发育不良的神经突无影响。在野生型小鼠中施用NMDA r拮抗剂可增强细胞增殖并降低新生神经元的存活。结论σ1R缺乏会通过下调NMDA rs来损害DG中的神经发生。

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