...
  • 主题
高级搜索  >
历史搜索 清空历史
首页> 外文期刊>The European Journal of Neuroscience >Calcium dynamics are altered in cortical neurons lacking the calmodulin-binding protein RC3.
【24h】

Calcium dynamics are altered in cortical neurons lacking the calmodulin-binding protein RC3.

机译：缺乏钙调蛋白结合蛋白RC3的皮质神经元中的钙动力学改变。

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

RC3 is a neuronal calmodulin-binding protein and protein kinase C substrate that is thought to play an important regulatory role in synaptic transmission and neuronal plasticity. Two molecules known to regulate synaptic transmission and neuronal plasticity are Ca(2+) and calmodulin, and proposed mechanisms of RC3 action involve both molecules. However, physiological evidence for a role of RC3 in neuronal Ca(2+) dynamics is limited. In the current study we utilized cultured cortical neurons obtained from RC3 knockout (RC3-/-) and wildtype mice (RC3+/+) and fura-2-based microscopic Ca(2+) imaging to investigate a role for RC3 in neuronal Ca(2+) dynamics. Immunocytochemical characterization showed that the RC3-/- cultures lack RC3 immunoreactivity, whereas cultures prepared from wildtype mice showed RC3 immunoreactivity at all ages studied. RC3+/+ and RC3-/- cultures were indistinguishable with respect to neuron density, neuronal morphology, the formation of extensive neuritic networks and the presence ofglial fibrillary acidic protein (GFAP)-positive astrocytes and gamma-aminobutyric acid (GABA)ergic neurons. However, the absence of RC3 in the RC3-/- neurons was found to alter neuronal Ca(2+) dynamics including baseline Ca(2+) levels measured under normal physiological conditions or after blockade of synaptic transmission, spontaneous intracellular Ca(2+) oscillations generated by network synaptic activity, and Ca(2+) responses elicited by exogenous application of N-methyl-D-aspartate (NMDA) or class I metabotropic glutamate receptor agonists. Thus, significant changes in Ca(2+) dynamics occur in cortical neurons when RC3 is absent and these changes do not involve changes in gross neuronal morphology or neuronal maturation. These data provide direct physiological evidence for a regulatory role of RC3 in neuronal Ca(2+) dynamics.
机译：RC3是一种神经元钙调蛋白结合蛋白和蛋白激酶C底物，被认为在突触传递和神经元可塑性中起重要的调节作用。已知调节突触传递和神经元可塑性的两个分子是Ca（2+）和钙调蛋白，RC3作用的拟议机制涉及这两个分子。但是，RC3在神经元Ca（2+）动态中的作用的生理证据是有限的。在当前的研究中，我们利用从RC3基因敲除（RC3-/-）和野生型小鼠（RC3 + / +）和呋喃2基显微镜Ca（2+）成像获得的皮质神经元来研究RC3在神经元Ca（ 2+）动态。免疫细胞化学表征显示RC3-/-培养物缺乏RC3免疫反应性，而从野生型小鼠制备的培养物在所有研究的年龄均显示RC3免疫反应性。 RC3 + / +和RC3-/-培养在神经元密度，神经元形态，广泛的神经网络形成以及胶质原纤维酸性蛋白（GFAP）阳性星形胶质细胞和γ-氨基丁酸（GABA）能神经元的存在方面没有区别。但是，在RC3-/-神经元中不存在RC3被发现会改变神经元Ca（2+）动力学，包括在正常生理条件下或在突触传递受阻，自发细胞内Ca（2+ ）网络突触活动和外源应用N-甲基-D-天冬氨酸（NMDA）或I类代谢型谷氨酸受体激动剂引起的Ca（2+）响应引起的振荡。因此，当缺少RC3时，皮质神经元中Ca（2+）动力学发生重大变化，并且这些变化不涉及总体神经元形态或神经元成熟的变化。这些数据为RC3在神经元Ca（2+）动态中的调节作用提供了直接的生理证据。

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