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

已知刺激诱导的细胞内Ca^2+浓度（[Ca^2+] i）升高以波的形式沿沿着细胞网络和上皮层传播，以协调细胞活动。与感觉末梢相连的胶质细胞通过其分支过程相互通信，构成连接轴突终末的网络。为了确定这些神经胶质细胞网中Ca2+信号的启动和传播机制，从大鼠触须中分离出监测毛发运动的披针形末梢，并通过延时共聚焦显微镜观察，同时通过用细玻璃针接触标本局部激活信号。还通过光漂白后荧光恢复技术（FRAP）和透射电子显微镜（TEM）评估了间隙连接的细胞间偶联。机械刺激引起覆盖在受扰的披针形神经胶质细胞突起内[Ca^<2+>] i的单峰升高，随后是延迟的胶质细胞内钙离子浓度的升高。 关于我们 在相邻的2到5个结尾的反应。这些次级信号中的一些起源于单个胶质细胞过程中的特定焦点，以向细胞体推进，而另一些则通过光学部分的近端进入过程。前者在刺激点周围的神经胶质过程中迅速扩散，涉及那些与接触细胞缺乏物理接触的神经胶质过程。后者，经过一段时间的延迟，影响的初级激活细胞的细胞质延伸与传播的信号偶尔进入相邻的神经胶质过程。只有前一种类型的细胞间信号被嘌呤受体阻断剂苏拉明灭活。FRAP实验和TEM观察表明，间隙连接通道，允许细胞质信使之间的运动胶质进程。这些研究结果表明，在感觉末梢，嘌呤诱导的神经胶质细胞的信号和那些潜在的依赖于细胞内的信使传播在自己的模式的空间扩展和时间过程中构成两种不同形式的受体轴突之间的通信。少

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