Сравнительная характеристика структурно-функциональных изменения поля СА 3 гиппокампа после острой ишемии и травмы головного мозга белых крыс

The aim of the study was to study pyramidal neurons and astrocytes of the hippocampal CA 3 region in dynamics in white rats after acute ischemia and severe traumatic brain injury. Material and methods. Acute ischemia was simulated by 20-minute occlusion of the common carotid arteries (CCA), and severe traumatic brain injury (TBI) by a free-falling weight impact. The Nissl staining, hematoxylin and eosin staining, immunohistochemical reactions for NSE, MAP-2, p38, GFAP were used in the study. The proliferative activity of the cells was assessed using the Ki-67 response. The study was carried out on thin (4 μm) serial frontal sections in the animals of the control group (animals without pathological factors, n=5) in 1, 3, 7 and 14 days after the experimental modeling of CCA occlusion (n=20) and TBI (n=20). Morphometric analysis was performed using the ImageJ 1.52s software. The relative area of edema-swelling zones in the neuropil, the number density of pyramidal neurons, the content of dystrophic and necrobiotically altered neurons, the content of neurons with one or more nucleoli, proliferating cells, the density of large trunks of pyramidal neurons dendrites, the total number density and the relative area of giant synaptic terminals in stratum lucidum was detected. The distribution of variation series, the verification of statistical hypotheses, and the construction of graphs were assessed using the Statistica 8.0 software and the R. Results. Mortality between groups did not differ and did not exceed 7%. In a day after CCA occlusion and TBI, there was a statistically significant increase in the relative volume of edema-swelling, the content of dystrophic and necrobiotically altered neurons, the total number density and the relative area of the terminals decreased, but the total number density of neurons did not change. In 3, 7 and 14 days, the mechanisms of neuroglio- and synaptic plasticity were activated. The content of neurons with two or more nucleoli increased, the total number and content of hypertrophied astrocytes increased, the cytoskeleton of damaged neurons was restored, and the content of interneuronal synapses increased. During the period from 3 to 14 days, the total number density of neurons in CCA occlusion decreased by 16.3%, and in TBI – by 33.7% (p=0.001). Pathological and compensatory-restorative changes were of a diffuse-focal nature and were more pronounced after TBI. Conclusion. Thus, the same type of focal heterochronous and heteromorphic dystrophic, necrobiotic and compensatory-restorative changes in the nervous tissue were observed after CCA occlusion and TBI in the hippocampal CA 3 region. Structural and functional recovery occurred together with a decrease in the total numerical density of pyramidal neurons and edema-swelling of the nervous tissue. More pronounced dystrophic and necrobiotic changes in TBI were combined with more pronounced compensatory-restorative changes in astrocytes and giant interneuronal synapses of the hippocampal CA 3 region. The revealed changes were considered as the basis for the standard permanent compensatory-restorative reorganization of the nervous tissue of the hippocampus in the postischemic and post-traumatic periods.