Long-lasting transneuronal changes in rat dentate granule cell dendrites after entorhinal cortex lesion. A combined intracellular injection and electron microscopy study
Long-lasting transneuronal changes in rat dentate granule cell dendrites after entorhinal cortex lesion. A combined intracellular injection and electron microscopy study
复制标题
DOI：
10.1111/j.1750-3639.1996.tb00846.x
复制
发表时间：
1996-07-01
期刊：
影响因子：
6.4
通讯作者：
Nitsch, R
中科院分区：
文献类型：
--
作者：
Diekmann, S;Ohm, TG;Nitsch, R
内嗅皮层损伤后，抑制性海马神经元表现为接受内嗅输入的树突持续稀疏。生理数据表明，在去内嗅海马中抑制和兴奋的长期不平衡。我们分析了去内嗅兴奋性大鼠颗粒细胞的细胞内染色树突状树。将对照组和单侧内嗅皮层损伤后存活2、8、60和270天的动物的颗粒细胞刺穿。对照细胞的树突具有典型的形状，追踪到海马裂，并通过EM分析确定树突的完整染料填充。相反，60和270天后病变，树突很少看到延伸到外部的分子层和树突的架构变得显着稀疏。损伤后60天，细胞内充满树突延伸到中分子层被类似胶质细胞的细胞簇包围。其中一些含有神经应用的染料，这表明细胞溶质室与改变树突的密切联系。这些观察到的变化超过了长时间的萌芽和从头突触形成的过程中剩余的传入。抑制性和兴奋性神经元的树突形态似乎需要来自内嗅皮层的特定输入。此外，发芽的剩余传入显然是不足以弥补这种损失的输入。
Following entorhinal cortex lesion, inhibitory hippocampal neurons show a persistent rarefication of those dendrites formally receiving entorhinal input. Physiological data indicate a long lasting disequilibrium of inhibition and excitation in the de-entorhinated hippocampus. We analyzed the intracellularly-stained dendritic tree of de-entorhinated excitatory rat granule cells. Granule cells of controls and animals surviving 2, 8, 60 and 270 days after unilateral entorhinal cortex lesion were impaled. Dendrites of control cells were of typical shape, traced to the hippocampal fissure and a complete dye filling of dendrites was ascertained by EM-analysis. Conversely, 60 and 270 days following lesioning, dendrites were only rarely seen to extend into the outer portions of the molecular layer and the dendritic architecture became significantly rarefied. Sixty days post-lesion, intracellularly filled dendrites extending to the middle molecular layer were surrounded by cell clusters resembling glia. Some of these contained the neuronally applied dye, suggesting a close association of the cytosolic compartments with the altered dendrites. These observed alterations exceed the process of sprouting and de novo synaptogenesis of remaining afference for long periods of time. The dendritic morphology of both inhibitory and excitatory neurons seems to require specific input from the entorhinal cortex. Moreover, sprouting of remaining afferents is apparently not sufficient to compensate for this loss of input.