![]() ![]() Control mice were also euthanized at the same age. Rabies-infected mice were sacrificed at the terminal stage of the disease. To evaluate the distribution of the protein NeuN in the motor cortex of normal and rabies-infected mice adult ICR mice were inoculated with rabies virus either intramuscularly or intracerebrally. The neuronal nuclear protein (NeuN) has become a widely used neuronal marker for the research and the histopathological diagnosis of nervous system diseases. The fatal outcome caused by rabies could be attributed to specific biochemical changes that severely impact neuronal function. Rabies is a lethal disease caused by a neurotropic virus that produces inconspicuous morphological changes hardly observable with conventional histopathology. These results lead us to postulate CRYAB as a possible marker of reactive astrogliosis in contused cortical tissue. Our results indicate a parallel behavior in the cellular expression of CRYAB and GFAP during the subacute response to TBI. The selective vulnerability of layer V of the cerebral cortex during TBI could explain the expression of CRYAB in neurons of this cortical layer. The only difference was the presence of a few pyramidal neurons that expressed CRYAB in layer V of the cerebral cortex. Most of the cells that overexpressed GFAP in the analyzed tissue also overexpressed CRYAB, a finding corroborated by the co-localization of the two markers. The histological expression of CRYAB was mainly seen in subcortical white matter astrocytes of injured tissue. Here, we used 3, 3'-diaminobenzidine (DAB) immunohistochemistry and immunofluorescence to verify CRYAB overexpression and to describe its expression and distribution in samples of contused cortical tissue derived from emergency decompressive surgery after severe TBI. Previous analyses of the gene expression profile in human brain contusion tissue showed us an exacerbated CRYAB overexpression. Crystallin alpha-B (CRYAB) is a molecular chaperone that apparently tries to stabilize the rapid thickening of the intermediate filaments of glial fibrillary acidic protein (GFAP) during the process of reactive astrogliosis in response to TBI. The pathophysiology of traumatic brain injury (TBI) has not yet been fully elucidated.
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