• 主题
高级搜索  >
历史搜索 清空历史
首页> 外文学位 >Neural nicotinic acetylcholine receptor and GAP-43 gene expression and regulation in the developing mammalian retina.
【24h】

Neural nicotinic acetylcholine receptor and GAP-43 gene expression and regulation in the developing mammalian retina.

机译：神经尼克烟碱乙酰胆碱受体和GAP-43基因在发育中的哺乳动物视网膜中的表达和调控。

获取原文
获取原文并翻译 | 示例
页面导航
  • 摘要
  • 著录项
  • 相似文献
  • 相关主题

摘要

uring development of the retina multipotential progenitor cells commit to a particular fate and differentiate into mature neurons. One of the earliest differentiations to take place in the developing retina is the formation of retinal ganglion cells (RGCs). The molecular mechanisms by which RGCs differentiate are unknown. One approach to this problem is to identify genes which are expressed during RGC differentiation and characterize their mechanisms of induction. We have taken this approach using genes encoding nicotinic acetylcholine receptors (nAChR) and the growth associated protein, GAP-43.;In situ hybridization assays were used to identify the temporal and spatial patterns of nAChR and GAP-43 gene expression in the developing retina. Both genes were induced around embryonic day 14 (E14) in recently born RGCs located at the vitreal surface. This corresponds to a time when RGC axons were growing towards their brain targets.;Based on these results, we hypothesized that either the environment the RGC axons traversed or their brain targets were initiating a signal that resulted in nAChR and GAP-43 gene expression. This hypothesis was tested by either transplanting E12 retinas to different brain environments or by explanting them into organ culture. The E12 retina was chosen since it represents a developmental time prior to RGC birth and therefore does not express nAChR or GAP-43 genes.;These studies showed that both transplanted and explanted retinae induce nAChR and GAP-43 genes on schedule. Therefore, neither the environment through which the RGC axon grows, nor its target is required for induction of nAChR or GAP-43 genes.;We investigated nAChR and GAP-43 gene expression in the ocular retardation mutant mouse,
机译：随着视网膜的发展，多能祖细胞决定了特定的命运并分化为成熟的神经元。视网膜发育中最早发生的分化之一是视网膜神经节细胞（RGC）的形成。 RGC分化的分子机制尚不清楚。解决该问题的一种方法是鉴定在RGC分化过程中表达的基因并表征其诱导机制。我们采用了编码烟碱样乙酰胆碱受体（nAChR）和生长相关蛋白GAP-43的基因;采用原位杂交法鉴定了nAChR和GAP-43基因在视网膜发育中的时空分布。这两个基因都是在位于玻璃体表面的最近出生的RGC中在胚胎第14天（E14）左右诱导的。这对应于RGC轴突向其大脑靶标生长的时间。基于这些结果，我们假设RGC轴突遍历的环境或其大脑靶标正在引发导致nAChR和GAP-43基因表达的信号。通过将E12视网膜移植到不同的大脑环境中或将其移植到器官培养物中来检验该假设。选择E12视网膜是因为它代表RGC出生之前的发育时间，因此不表达nAChR或GAP-43基因。这些研究表明，移植的视网膜和移植的视网膜均能按计划诱导nAChR和GAP-43基因。因此，诱导nAChR或GAP-43基因既不需要RGC轴突生长的环境，也不是其靶标。我们研究了nAChR和GAP-43基因在弱视突变小鼠中的表达，

著录项

  • 作者

    Hoover, Frank.;

  • 作者单位

    University of Michigan.;

  • 授予单位 University of Michigan.;
  • 学科 Biology Neuroscience.;Biology Anatomy.;Biology Molecular.
  • 学位 Ph.D.
  • 年度 1992
  • 页码 214 p.
  • 总页数 214
  • 原文格式 PDF
  • 正文语种 eng
  • 中图分类
  • 关键词

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