首页> 外文期刊>The European Journal of Neuroscience >Elevated zinc transporter ZnT3 in the dentate gyrus of mast cell-deficient mice
【24h】

Elevated zinc transporter ZnT3 in the dentate gyrus of mast cell-deficient mice

机译:升高的锌转运蛋白ZnT3在肥大细胞缺乏小鼠的牙齿过滤中

获取原文
获取原文并翻译 | 示例
           

摘要

Zinc is important in neurogenesis, but excessive levels can cause apoptosis and other pathologies leading to cognitive impairments. Mast cells are present in many brain regions including the hippocampus, an area rich in vesicular zinc. Mast cells contain zinc-rich granules and a well-developed mechanism for uptake of zinc ions; both features point to the potential for a role in zinc homeostasis. Prior work using the Timm stain supported this hypothesis, as increased labile zinc was detected in the hippocampus of mast cell-deficient mice compared to wild-type mice while no differences in total zinc were found between the two genotypes in the whole brain or other tissues. The current report further examines differences in zinc homeostasis between wild-type and mast cell-deficient mice by exploring the zinc transporter ZnT3, which transports labile zinc into synaptic vesicles. The first study used immunocytochemistry to localize ZnT3 within the mossy fibre layer of the hippocampus to determine whether there was differential expression of ZnT3 in wild-type versus mast cell-deficient mice. The second study used inductively coupled plasma mass spectrometry (ICP-MS) to determine total zinc content in the whole dentate gyrus of the two genotypes. The immunocytochemical results indicate that there are higher levels of ZnT3 localized to the mossy fibre layer of the dentate gyrus of mast cell-deficient mice than in wild-type mice. The ICP-MS data reveal no differences in total zinc in dentate gyrus as a whole. The results are consistent with the hypothesis that mast cells participate in zinc homeostasis at the level of synaptic vesicles.
机译:锌在神经发生中很重要,但水平过量会导致细胞凋亡和其他病理导致认知障碍。肥大细胞存在于包括海马的许多脑区域中,该区域富含囊泡锌。肥大细胞含有富含锌的颗粒和一种用于摄取锌离子的良好发达的机制;这两个特征都指出锌稳态中作用的潜力。使用TIMM染色的工作支持这一假设,与粪便细胞缺陷小鼠的海马在野生型小鼠的海马中检测到的不稳定锌,而全部大脑或其他组织的两种基因型之间没有发现总锌的差异。目前的报告通过探索锌转运蛋白ZnT3,进一步研究了野生型和肥大细胞缺乏小鼠之间的锌稳态差异,所述锌转运蛋白ZnT3将不稳定的锌转化为突触囊泡。第一研究使用免疫细胞化学来定位海马苔藓纤维层内的ZnT3,以确定源型与肥大细胞缺陷小鼠是否存在差异的ZnT3。第二种研究使用电感耦合等离子体质谱(ICP-MS)以确定两种基因型的整个牙齿过度的总锌含量。免疫细胞化学结果表明,含有较高水平的ZnT3局部化为肥大细胞缺乏小鼠的牙齿缺乏小鼠的牙脂纤维层的猪纤维层。 ICP-MS数据揭示了整个牙齿回形图中总锌的差异。结果与肥大细胞在突触囊泡水平上参与锌稳态的假设一致。

著录项

相似文献

  • 外文文献
  • 中文文献
  • 专利
获取原文

客服邮箱:kefu@zhangqiaokeyan.com

京公网安备:11010802029741号 ICP备案号:京ICP备15016152号-6 六维联合信息科技 (北京) 有限公司©版权所有
  • 客服微信

  • 服务号