Deller T, Frotscher M
Institute of Anatomy, University of Freiburg, Germany.
Prog Neurobiol. 1997 Dec;53(6):687-727. doi: 10.1016/s0301-0082(97)00044-0.
In response to a central nervous system trauma surviving neurons reorganize their connections and form new synapses that replace those lost by the lesion. A well established in vivo system for the analysis of this lesion-induced plasticity is the reorganization of the fascia dentata following unilateral entorhinal cortex lesions in rats. After general considerations of neuronal reorganization following a central nervous system trauma, this review focuses on the sprouting of single fibres in the rat hippocampus after entorhinal lesion and the molecular factors which may regulate this process. First, the connectivity of the fascia dentata in control animals is reviewed and previously unknown commissural fibers to the outer molecular layer and entorhinal fibres to the inner molecular layer are characterized. Second, sprouting of commissural and crossed entorhinal fibres after entorhinal cortex lesion is described. Single fibres sprout by forming additional collaterals, axonal extensions, boutons, and tangle-like axon formations. It is pointed out that the sprouting after entorhinal lesion mainly involves unlesioned fibre systems terminating within the layer of fibre degeneration and is therefore layer-specific. Third, molecular changes associated with axonal growth and synapse formation are considered. In this context, the role of adhesion molecules, glial cells, and neurotrophic factors for the sprouting process are discussed. Finally, an involvement of sprouting processes in the formation of neuritic plaques in Alzheimer's disease is reviewed and discussed with regard to the axonal tangle-like formations observed after entorhinal cortex lesion.
为应对中枢神经系统创伤，存活的神经元会重新组织其连接并形成新的突触，以取代因损伤而丧失的突触。一个用于分析这种损伤诱导可塑性的成熟体内系统是大鼠单侧内嗅皮层损伤后齿状回的重组。在对中枢神经系统创伤后的神经元重组进行一般性考虑之后，本综述重点关注内嗅损伤后大鼠海马中单纤维的出芽以及可能调节这一过程的分子因素。首先，回顾了对照动物中齿状回的连接性，并对以前未知的到外分子层的连合纤维和到内分子层的内嗅纤维进行了特征描述。其次，描述了内嗅皮层损伤后连合纤维和交叉内嗅纤维的出芽情况。单纤维通过形成额外的侧支、轴突延伸、终扣和缠结状轴突结构而出芽。需要指出的是，内嗅损伤后的出芽主要涉及终止于纤维变性层内的未损伤纤维系统，因此具有层特异性。第三，考虑了与轴突生长和突触形成相关的分子变化。在此背景下，讨论了黏附分子、胶质细胞和神经营养因子在出芽过程中的作用。最后，综述并讨论了出芽过程在阿尔茨海默病神经炎性斑块形成中的作用，并将其与内嗅皮层损伤后观察到的轴突缠结状结构进行了比较。
