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腱生蛋白-R可诱导沿神经突轴形成富含肌动蛋白的微突起和分支。

Tenascin-R induces actin-rich microprocesses and branches along neurite shafts.

作者信息

Zacharias Ute, Leuschner Roland, Nörenberg Ursel, Rathjen Fritz G

机构信息

Max-Delbrück-Centrum für Molekulare Medizin, Robert-Rössle-Strasse 10, D-13092 Berlin, Germany.

出版信息

Mol Cell Neurosci. 2002 Dec;21(4):626-33. doi: 10.1006/mcne.2002.1203.

Abstract

The formation of protrusions along the shaft of neurites might be important in the establishment and refinement of neuronal connections during development. In a search for extracellular signals that affect the formation of microprocesses along neurites we found that the ECM glycoprotein tenascin-R (TN-R) but not other ECM glycoproteins increased the percentage of tectal neurons with actin-rich microprocesses and side branches. Longer actin-based microprocesses were also invaded by microtubuli in their proximal part. The formation of microprocesses by TN-R extending laterally along the neuritic shaft was time- and dose-dependent. In addition to the induction of microprocesses, TN-R increased the size of the growth cone of tectal neurons. A cross-species experiment in combination with blocking antibodies demonstrated that the TN-R-induced effects are mediated by the Ig superfamily member contactin. These observations suggest that TN-R via its neuronal receptor contactin might induce a transition from long-distance growth of tectal interneurons to differentiation, including the formation of microprocesses.

摘要

神经突轴上突起的形成在发育过程中神经元连接的建立和完善中可能很重要。在寻找影响神经突上微突起形成的细胞外信号时,我们发现细胞外基质糖蛋白腱生蛋白-R(TN-R)而非其他细胞外基质糖蛋白增加了具有富含肌动蛋白的微突起和侧支的视顶盖神经元的比例。较长的基于肌动蛋白的微突起在其近端部分也被微管侵入。TN-R沿神经突轴横向延伸形成微突起是时间和剂量依赖性的。除了诱导微突起形成外,TN-R还增加了视顶盖神经元生长锥的大小。一项跨物种实验与阻断抗体相结合表明,TN-R诱导的效应是由免疫球蛋白超家族成员接触蛋白介导的。这些观察结果表明,TN-R通过其神经元受体接触蛋白可能诱导视顶盖中间神经元从长距离生长向分化的转变,包括微突起的形成。

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