The reorganization of the dentate gyrus of the hippocampus and changes in mitochondrial fission were evaluated using the kainate model of temporal lobe epilepsy. In 28 days after administration of 0.5 μg kainic acid, disturbances in the distribution of neuronal precursors in the subgranular zone of the hippocampus, thickening of the granular layer, and an increase in the content of synaptophysin in the molecular layer were detected.
View Article and Find Full Text PDFData on the participation of microbiota in the development of Parkinson's disease allow us to discuss the ability of bacterial preparations to influence the processes leading to neurodegeneration. We studied the effect of oral administration of Limosilactobacillus fermentum U-21 lyophilisate on a model of Parkinson's disease in rats induced by combined intranigral injection of LPS and systemic administration of paraquat. The toxins significantly increased the number of missteps in the "narrowing beam walking" test, but a tendency to a decrease in this parameter was shown after treatment with U-21.
View Article and Find Full Text PDFA comparative assessment of the expression of the mitochondrial fission marker Drp1 and the autophagy marker LC3 in neurons and endothelial cells in the hippocampus and entorhinal cortex during progression of cognitive deficit was performed in animals with intrahippocampal administration of β-amyloid. In both brain regions, the expression of Drp1 and LC3 in neuronal and endothelial cells was enhanced. The peak of cognitive impairment corresponded to the maximum expression of Drp1 and LC3 in hippocampal neurons and was preceded by an increase in the number of Drp1 and LC3 endothelial cells in this brain region.
View Article and Find Full Text PDFSixty and 90 days after unilateral intranigral injection of LPS to Wistar rats (10 μg), activation of microglia, neuronal death, and formation of synuclein-positive inclusions were observed in the substantia nigra, but not in dopaminergic neurons. Astrocytes were characterized by increased expression of gliofibrillary protein GFAP, vimentin, complement protein C3, aquaporin-4, and connexin-43. At later stages, GFAP expression decreased, but the distribution of aquaporin-4 and connexin-43 remained disordered, and neuronal degeneration deteriorated.
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