Neuro-Glio-Vascular Complexes of the Brain After Acute Ischemia

The purpose of the study is to compare the structural and functional state of neuro-glio-vascular microstructural complexes of the somatosensory cortex (SSC), CA1 of the hippocampus and amygdala of the brain of white rats under normal conditions and after acute ischemia caused by a 20-minute occlusion of common carotid arteries. Materials and methods. In this experiment, neurons, astrocytes, endotheliocytes, pericytes, basal membrane of the microvessels were studied in the normal (n=5) and the reperfusion period (1, 3, 7, 14, 21 and 30 days, n=30) using electron and fluorescence microscopy (DAPI staining). The morphometric analysis was carried out using the ImageJ 1.46 software. Results. During the recovery period after ischemia was noted reactive (edema-swelling, tinctorial properties of cells) and compensatory-restoration (hyperplasia, hypertrophy, proliferation, increased transcytosis) changes in neuro-glia-vascular complexes. After ischemia, the number of neurons decreased (by 8.7%—55,3%), and the glial cell count 2—3 fold increased. Increasing neuroglial index (NGI) was accompanied by: 1) the emergence of microvessels with numerous branched processes of pericytes, 2) the complication of the spatial organization of basal membranes, and 3) the structural features of activation of transcytosis processes (large number of caveolae, smooth and clathrin vesicles, large vesicles) in pericytes and endothelial cells. Conclusion. These findings indicate the compensatory-restoration changes in the components of neuro-gliovascular complexes SSC, CA1 of the hippocampus and amygdala of white rat’s brain after a 20-minute occlusion of the common carotid arteries. The most complete implementation of mechanisms for the protection and repair of damaged neurons occurs in the SSC and amygdala exhibiting high NGI values.