...
  • 主题
高级搜索  >
历史搜索 清空历史
首页> 外文期刊>Frontiers in neuroendocrinology >Oxytocin-secreting neurons: A physiological model of morphological neuronal and glial plasticity in the adult hypothalamus.
【24h】

Oxytocin-secreting neurons: A physiological model of morphological neuronal and glial plasticity in the adult hypothalamus.

机译：催产素分泌神经元：成年下丘脑形态神经元和神经胶质可塑性的生理模型。

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

Oxytocin-secreting neurons of the hypothalamoneurohypophysial system undergo reversible morphological changes whenever they are strongly stimulated. In the hypothalamus, such structural plasticity is represented by modifications in the size and shape of their somata and dendrites, in the extent to which their surfaces are covered by glia, and in the density of their synapses. In the neurohypophysis, there is a parallel reduction in glial (pituicyte) coverage of their axons together, with retraction of pituicyte processes from the perivascular basal lamina and an increase in the number and size of their terminals. These changes occur rapidly, within a few hours. On the other hand, the system returns to its prestimulated condition on arrest of stimulation at a rate that depends on the length of time it has remained activated. Such neuronal-glial changes have several functional consequences. In the hypothalamic nuclei, reduction in astrocytic coverage of oxytocinergic neurons and their synapses modifies extracellular ionic homeostasis and glutamate clearance and, therefore, their overall excitability. Since it results in extensive dendritic bundling, it may also lead to ephaptic interactions and may facilitate dendritic electrotonic coupling. A most important indirect effect may be to permit synaptic remodeling that occurs concomitantly and that results in significant increases in the number of excitatory and inhibitory synapses driving their activity. In the stimulated neurohypophysis, glial retraction results in increased levels of extracellular K+ which can enhance neurohormone release while an enlarged neurovascular contact zone may facilitate diffusion of neurohormone into the circulation. Ongoing work aims to unravel the cell mechanisms and factors underlying such plasticity and has revealed that neurons and glia of the hypothalamoneurohypophysial system continue to express juvenile molecular features associated with similar neuronglial interactions and synaptic events during development and regeneration. They include strong expression of cell surface adhesion molecules like F3/contactin and polysialylated neural cell adhesion molecule, extracellular matrix glycoproteins like tenascin C, and cytoskeletal proteins like vimentin and microtubule-associated protein 1D. Some of these molecules reach the cell surface constitutively while others follow the activity-dependent regulated pathway. We consider many of these molecular features permissive, allowing oxytocin neurons and their glia to undergo morphological remodeling throughout life, provided the proper stimulus intervenes. In the hypothalamic nuclei, one such stimulus is centrally released oxytocin; in the neurohypophysis, an adrenergic, cAMP-mediated mechanism appears responsible.
机译：下丘脑神经下垂体系统分泌催产素的神经元在受到强烈刺激时会发生可逆的形态变化。在下丘脑中，这种结构可塑性通过其躯体和树突的大小和形状的改变，其表面被神经胶质覆盖的程度以及突触的密度来表示。在神经垂体中，其轴突的神经胶质（皮细胞）覆盖范围平行减少，皮膜细胞突从血管周围基底层中撤出，末端数量和大小增加。这些变化会在几个小时内迅速发生。另一方面，系统在停止刺激时以其保持激活时间长度的速率返回到其预刺激状态。这种神经胶质改变具有若干功能后果。在下丘脑核中，催产素能神经元及其突触的星形胶质细胞覆盖率降低，会改变细胞外离子稳态和谷氨酸清除率，从而改变其总体兴奋性。由于它导致广泛的树突状束缚，因此它也可能导致脑神经相互作用，并可能促进树突状的电声耦合。最重要的间接影响可能是允许同时发生的突触重塑，并导致驱动其活动的兴奋性和抑制性突触数量大量增加。在刺激的神经垂体中，神经胶质退缩导致细胞外K +水平升高，这可以增强神经激素的释放，而扩大的神经血管接触区则可能促进神经激素向循环中的扩散。正在进行的工作旨在揭示这种可塑性背后的细胞机制和因素，并揭示了下丘脑神经下垂体系统的神经元和神经胶质继续表达与发育和再生过程中类似的神经胶质相互作用和突触事件相关的少年分子特征。它们包括细胞表面粘附分子（例如F3 / contactin和多唾液酸化的神经细胞粘附分子），胞外基质糖蛋白（例如腱糖蛋白C）以及细胞骨架蛋白（例如波形蛋白和微管相关蛋白1D）的强表达。这些分子中的一些组成性地到达细胞表面，而其他分子遵循活性依赖的调节途径。我们认为许多这些分子特征是允许的，只要适当的刺激干预，催产素神经元及其神经胶质就可以在一生中经历形态重塑。在下丘脑核中，一种这样的刺激是中央释放的催产素。在神经垂体中，肾上腺素，cAMP介导的机制似乎起作用。

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