Miller P D, Styren S D, Lagenaur C F, DeKosky S T
Department of Neurobiology, University of Pittsburgh School of Medicine, Pennsylvania.
J Neurosci. 1994 Jul;14(7):4217-25. doi: 10.1523/JNEUROSCI.14-07-04217.1994.
We evaluated the immunohistological changes in neural cell adhesion molecule (N-CAM) expression in the adult rat dentate gyrus during the period of synaptic degeneration, axonal sprouting, and synaptogenesis following ipsilateral entorhinal cortex (ERC) lesion. This lesion denervates the outer two-thirds of the dentate granule cells dendrites and induces compensatory sprouting from the subjacent inner one-third into the denervated zone, as well as reactive synaptogenesis in the denervated outer molecular layer. In unlesioned adult hippocampus, antibodies to total N-CAM stained the inner molecular layer intensely, and the outer molecular layer (ML) more lightly. After ERC lesion the intense staining of the inner layer widened, the expansion following the known temporal sequence of commissural and associational (C/A) axon sprouting into the denervated zone. In normal unlesioned controls there was very light, uniform staining of the ML with antibodies directed against embryonic N-CAM (eN-CAM). By 2 d post-ERC lesion, the outer two-thirds of the ML stained robustly with antibody to eN-CAM. This area of intense staining receded as the C/A axon collaterals from the inner one-third entered the denervated zone, so that by 30 d the intense eN-CAM staining only occupied the outer half of the ML. The increased expression of eN-CAM remained present at 60 d post-ERC lesion, past the point that synaptic volume density has returned to normal levels in the denervated zone. Ultrastructural studies showed that the newly expressed eN-CAM was located on the surface of dendrites in the denervated zone, but was not found at the synaptic contacts.(ABSTRACT TRUNCATED AT 250 WORDS)
我们评估了成年大鼠齿状回中神经细胞黏附分子(N-CAM)表达的免疫组织学变化,该变化发生在同侧内嗅皮质(ERC)损伤后的突触退化、轴突发芽和突触形成阶段。这种损伤使齿状颗粒细胞树突的外三分之二失去神经支配,并诱导相邻内三分之一向失神经支配区域进行代偿性发芽,以及在失神经支配的外分子层中发生反应性突触形成。在未损伤的成年海马体中,针对总N-CAM的抗体强烈染色内分子层,而外分子层(ML)染色较浅。ERC损伤后,内层的强烈染色变宽,其扩展遵循已知的连合和联合(C/A)轴突发芽进入失神经支配区域的时间顺序。在正常未损伤的对照中,针对胚胎N-CAM(eN-CAM)的抗体对ML的染色非常浅且均匀。在ERC损伤后2天,ML的外三分之二用抗eN-CAM抗体强烈染色。随着来自内三分之一的C/A轴突侧支进入失神经支配区域,这个强烈染色的区域逐渐消退,因此到30天时,强烈的eN-CAM染色仅占据ML的外半部分。在ERC损伤后60天,eN-CAM的表达增加仍然存在,此时失神经支配区域的突触体积密度已恢复到正常水平。超微结构研究表明,新表达的eN-CAM位于失神经支配区域树突的表面,但在突触接触处未发现。(摘要截断于250字)