Аннотация
The aim of the study was to investigate the cytoarchitectonic dynamics and cause-and-effect relationships between changes in layers III and V of the sensorimotor cortex of white rats during chronic cerebral ischemia. Material and methods. Chronic cerebral ischemia was modeled in 72 male Wistar rats by bilateral ligation of the common carotid arteries. Animals were sacrificed at the control time and after 30, 90, 150, 210, and 270 days (n=6 in each group). Histological and morphometric examination of frontal sections of layers III and V was performed using Nissl staining. Statistical processing was performed using single-factor, correlation, regression, and lag analysis using both parametric and nonparametric criteria. Results. Statistically significant specific differences in the dynamics of neurodegenerative changes were found in layers III and V. In layer III, a nonlinear, wave-like dynamics of the total numerical density of neurons and the numerical density of normochromic neurons was revealed with a pronounced decrease on the 30th day (40.6±1.9 versus 70.7±2.1 in the control and 14.2±0.6 versus 67.3±1.4 in the control; p<0.001), followed by partial recovery by the 150th day and repeated deterioration by the 270th day. In layer V, the changes were less pronounced and were predominantly linear. A strong positive correlation was found between of the total numerical density of neurons and the numerical density of normochromic neurons within each layer (layer III: r=0.78; layer V: r=0.85; p<0.001 for both). Regression and lag analyses confirmed the cascade nature of cytoarchitectonic reorganization: changes in layer III statistically significantly predicted subsequent changes in layer V (β=0.287, p=0.003 for the numerical density of normochromic neurons). Conclusion. Chronic ischemia causes a cascade of neurodegeneration that initiates in the upper parvocellular layer III and involves the underlying layer V. The identified specific patterns of damage in layers III and V of the sensorimotor cortex are of key importance for better understanding the pathogenesis of ischemic brain lesions and can serve as a basis for the development of neuroprotective strategies.