Lehmann S, Kuchler S, Gobaille S, Marschal P, Badache A, Vincendon G, Zanetta J P
Laboratoire de Neurobiologie Moléculaire des Interactions Cellulaires, CNRS UPR A 0416, Strasbourg, France.
Brain Res Bull. 1993;30(3-4):515-21. doi: 10.1016/0361-9230(93)90286-k.
It has been previously shown that sectioning of parallel fibers in the cerebellar molecular layer of adult rats gave rise to rapid reinnervation of the target cells, i.e., Purkinje cells. This paper reports that such a reinnervation is accompanied by reexpression (partial and total) of two developmentally regulated complementary molecules. These are an endogenous mannose-binding lectin, called R1, which reappears at the surface of the dendrites of Purkinje cells, and an endogenous glycoprotein ligand of R1, the 31 kDa glycoprotein, which seems to be neosynthetized and transported to the surface of parallel fibers. In this system, embryonic N-CAM is not reexpressed in neurons but reappears in reactive astrocytes in the vicinity of the lesion. The reexpression of recognition molecules (lectin and glycoprotein ligand) involved in normal synaptogenesis, may constitute the molecular basis for repair of nervous circuits in the adult as well.
先前的研究表明，切断成年大鼠小脑分子层中的平行纤维会导致靶细胞（即浦肯野细胞）迅速重新获得神经支配。本文报道，这种重新神经支配伴随着两种受发育调控的互补分子的重新表达（部分和完全）。它们是一种内源性甘露糖结合凝集素，称为R1，它重新出现在浦肯野细胞树突表面，以及R1的一种内源性糖蛋白配体，即31 kDa糖蛋白，它似乎是新合成并转运到平行纤维表面的。在这个系统中，胚胎N-CAM在神经元中不会重新表达，而是在损伤附近的反应性星形胶质细胞中重新出现。参与正常突触形成的识别分子（凝集素和糖蛋白配体）的重新表达，也可能构成成年期神经回路修复的分子基础。
