...
  • 主题
高级搜索  >
历史搜索 清空历史
首页> 外文期刊>Biology Open >Olfactory ensheathing glia are required for embryonic olfactory axon targeting and the migration of gonadotropin-releasing hormone neurons
【24h】

Olfactory ensheathing glia are required for embryonic olfactory axon targeting and the migration of gonadotropin-releasing hormone neurons

机译：嗅鞘神经胶质是胚胎嗅轴突靶向和促性腺激素释放激素神经元迁移所必需的

获取原文
           
页面导航
  • 摘要
  • 著录项
  • 相似文献
  • 相关主题

摘要

Kallmann's syndrome is caused by the failure of olfactory axons and gonadotropin-releasing hormone (GnRH) neurons to enter the embryonic forebrain, resulting in anosmia and sterility. Sox10 mutations have been associated with Kallmann's syndrome phenotypes, but their effect on olfactory system development is unknown. We recently showed that Sox10 is expressed by neural crest-derived olfactory ensheathing cells (OECs). Here, we demonstrate that in homozygous Sox10lacZ/lacZ mouse embryos, OEC differentiation is disrupted; olfactory axons accumulate in the ventromedial olfactory nerve layer and fewer olfactory receptor neurons express the maturation marker OMP (most likely owing to the failure of axonal targeting). Furthermore, GnRH neurons clump together in the periphery and a smaller proportion enters the forebrain. Our data suggest that human Sox10 mutations cause Kallmann's syndrome by disrupting the differentiation of OECs, which promote embryonic olfactory axon targeting and hence olfactory receptor neuron maturation, and GnRH neuron migration to the forebrain.
机译：Kallmann综合征是由嗅轴突和促性腺激素释放激素（GnRH）神经元进入胚胎前脑衰竭引起的，从而导致失眠和不育。 Sox10突变已与Kallmann综合征表型相关联，但它们对嗅觉系统发育的影响尚不清楚。我们最近显示，Sox10由神经c衍生的嗅鞘细胞（OEC）表达。在这里，我们证明在纯合的Sox10lacZ / lacZ小鼠胚胎中，OEC分化受到破坏;嗅轴突聚集在腹侧嗅神经层中，较少的嗅觉受体神经元表达成熟标记物OMP（最可能是由于轴突靶向失败）。此外，GnRH神经元在周围聚集在一起，较小的一部分进入前脑。我们的数据表明，人的Sox10突变可通过破坏OEC的分化而引起Kallmann综合征，这会促进胚胎嗅轴突靶向并因此促使嗅觉受体神经元成熟以及GnRH神经元迁移至前脑。

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