权益分类	功能权益	普通用户	{{item.name}}会员
{{category.name}}	{{benefitItem.name}}

Mechanisms for initiation and propagation of calcium signals in glial nets associated with sensory endings: morphological and molecular analysis.

与感觉末梢相关的神经胶质网中钙信号的启动和传播机制：形态学和分子分析。

基本信息

批准号：
17590143
负责人：
IWANAGA Hiromi
金额：
$ 2.37万
依托单位：
HOKKAIDO UNIVERSITY
依托单位国家：
日本
项目类别：
Grant-in-Aid for Scientific Research (C)
财政年份：
2005
资助国家：
日本
起止时间：
2005 至 2006
项目状态：
已结题

项目摘要

Stimulus-induced elevations in the intracellular Ca^<2+> concentration ([Ca^<2+>]_i) are known to propagate as waves along cell networks and epithelial sheets for coordination of cell activities. Glial cells associating with sensory endings communicate with one another by their branching processes to constitute networks connecting axon terminals. In order to define the mechanism of initiation and propagation of Ca2+ signals in these glial nets, lanceolate endings that monitor hair movements, were isolated from rat vibrissae, and observed by time-lapse confocal microscopy while the signaling was locally activated by touching the specimen with a fine glass needle. Intercellular coupling by gap junctions was also assessed by the technique of fluorescence recovery after photobleaching (FRAP) and by transmission electron microscopy (TEM). Mechanical stimuli which induced a single-peaked [Ca^<2+>]_i elevation in glial processes covering the perturbed lanceolate were followed by delayed glial … More responses in neighboring 2 to 5 endings. Some of these secondary signals originated from a specific focus in individual glial processes to advance toward the cell body, while others entered the processes through the proximal end of the optical section. The former rapidly spread among glial processes around the stimulation point to involve those lacking physical contacts with the touched cell. The latter, after a delay, affected cytoplasmic extensions of the primarily-activated cell with the propagated signals occasionally traveling into an adjacent glial process. Only the former type of intercellular signaling was inactivated by the purinoceptor blocker suramin. FRAP experiments and TEM observations demonstrated gap junction channels which allow movement of cytoplasmic messengers between the glial processes. These findings indicate that in sensory endings, purinergically-induced glial signals and those potentially dependent on an intracellular messenger are propagated in their own patterns of spatial expansion and time courses to constitute two distinct forms of communication among the receptor axons. Less

众所周知，刺激诱导的细胞内钙离子浓度升高([Ca^&lt；2+&gt；]_i)以波的形式沿细胞网络和上皮层传播，以协调细胞活动。与感觉末梢相关的神经胶质细胞通过它们的分支过程相互联系，构成连接轴突终末的网络。为了明确钙信号在这些神经胶质网络中的启动和传播机制，从大鼠触须中分离出监测毛发运动的披针形终末，并用时间推移共聚焦显微镜观察，同时用细小的玻璃针接触标本来局部激活信号。用荧光漂白恢复技术(FRAP)和透射电子显微镜(TEM)检测缝隙连接对细胞间偶联的影响。机械刺激在被扰动的披针形突起上引起单峰的[Ca^&lt；2+]_i升高，随后是延迟的神经胶质…在相邻的2到5个结尾中有更多的回复。这些次级信号中的一些来自个别神经胶质突起中的特定焦点，向细胞体前进，而另一些则通过光学部分的近端进入突起。前者在刺激点周围的神经胶质突起中迅速扩散，涉及那些与被触摸细胞缺乏物理接触的人。后者在延迟一段时间后，影响最初激活的细胞的细胞质延伸，传播的信号偶尔会进入邻近的神经胶质突起。只有前一种细胞间信号被嘌呤受体阻滞剂苏拉明灭活。FRAP实验和透射电子显微镜观察表明，缝隙连接通道允许细胞质信使在神经胶质突起之间移动。这些发现表明，在感觉终末，嘌呤诱导的神经胶质信号和那些可能依赖于细胞内信使的信号以各自不同的空间扩展和时间进程模式传播，构成了感受器轴突之间两种不同形式的通信。较少