Porras Andrés Obdulio, Morales María Paula, Santamaría Gerardo, Torres-Fernández Orlando
Grupo de Morfología Celular, Instituto Nacional de Salud (INS), Av. Calle 26 No. 51-20, Bogotá, DC, 111321, Colombia.
J Mol Histol. 2024 Dec 30;56(1):62. doi: 10.1007/s10735-024-10348-5.
The effect of rabies virus infection on dendritic morphology and on the expression of the MAP2 protein in Purkinje cells in the cerebellum of mice was studied. ICR mice were inoculated with rabies virus, and six days later, the mice were sacrificed, the cerebellum was removed and processed for Golgi-Cox staining or MAP2 immunohistochemistry. Infection with rabies virus altered the dendritic pattern of Purkinje cells ranged from moderate changes to accentuated retraction in the dendritic tree of some Purkinje cells. The loss of dendritic branches in the samples of mice infected with RABV was also reflected in a decrease in intersections quantified using the Sholl technique, thus suggesting dendritic pathology. Immunoreactivity to MAP2 protein in the molecular layer of the cerebellum of control mice was mainly distributed in dendrites of Purkinje cells. Some somas were faintly stained. In infected mice immunoreactivity to MAP2 was intense in somas and dendrites of Purkinje cells and in some interneurons. These results are consistent with similar findings we previously reported for the cerebral cortex and spinal cord of rabies-infected mice. But they differ from studies in other pathologies where an association between dendritic pathology and loss of MAP2 immunoreactivity has been found. Our studies in rabies contribute to suggestion that MAP2 overexpression may also be associated with alterations in dendritic morphology. MAP2 protein contributes to maintaining cytoskeleton stability. However, in rabies, increased MAP2 expression here only determined by immunohistochemistry could destabilize the cytoskeleton of dendrites. Golgi staining is considered the gold standard for the study of dendritic morphology. Its association with changes in MAP2 expression appears to provide molecular support for the concept of dendritic pathology. These results contribute to the understanding of the effect of rabies virus infection on dendritic morphology. They therefore reinforce the idea that rabies not only has a dysfunctional effect on neurons, as some authors claim, but also affects their structure.
研究了狂犬病病毒感染对小鼠小脑浦肯野细胞树突形态及微管相关蛋白2(MAP2)表达的影响。将狂犬病病毒接种于ICR小鼠,6天后处死小鼠,取出小脑并进行高尔基-考克斯染色或MAP2免疫组织化学处理。狂犬病病毒感染改变了浦肯野细胞的树突模式,从一些浦肯野细胞树突树的中度变化到明显回缩。狂犬病病毒(RABV)感染小鼠样本中树突分支的减少也反映在使用肖尔技术量化的交叉点减少上,从而提示树突病变。对照小鼠小脑分子层中对MAP2蛋白的免疫反应性主要分布在浦肯野细胞的树突中。一些胞体染色较淡。在感染小鼠中,浦肯野细胞的胞体和树突以及一些中间神经元中对MAP2的免疫反应性很强。这些结果与我们之前报道的狂犬病感染小鼠大脑皮层和脊髓的类似发现一致。但它们与其他病理学研究不同,在其他病理学研究中发现了树突病变与MAP2免疫反应性丧失之间的关联。我们对狂犬病的研究表明,MAP2过表达也可能与树突形态改变有关。MAP2蛋白有助于维持细胞骨架的稳定性。然而,在狂犬病中,此处仅通过免疫组织化学确定的MAP2表达增加可能会破坏树突的细胞骨架稳定性。高尔基染色被认为是研究树突形态的金标准。它与MAP2表达变化的关联似乎为树突病变的概念提供了分子支持。这些结果有助于理解狂犬病病毒感染对树突形态的影响。因此,它们强化了这样一种观点,即狂犬病不仅像一些作者所声称的那样对神经元有功能障碍作用,而且还会影响其结构。