Quantitative morphological characteristics of changes in the hippocampal dentate gyrus in rats with various neurocognitive disorders after severe traumatic brain injury

Background. In solving numerous issues related to the treatment and rehabilitation of patients with traumatic brain injury, it is of particular interest to study the pathomorphological mechanisms that determine the nature of the formation and dynamics of neurocognitive disorders at various times after the injury. The study aims to determine the tissue and cellular posttraumatic changes in the structure of the cerebral dentate cortex of rats with various neurocognitive disorders at different times after severe traumatic brain injury. Methods. A "shock acceleration model" was used to reproduce severe traumatic brain injury in rats. According to the results of neurological tests, the rats were divided into three groups: 1) the first – animals after trauma with neurocognitive disorders and memory disorders; 1) the second – animals after trauma with neurocognitive disorders without memory disorders; 3) comparison group – animals after trauma without neurocognitive disorders. A histological, morphometric and immunohistochemical study of the cerebral dentate cortex was carried out using the markers β-tubulin, Synaptophysin, GAP43, NCAM1, N-cadherin, GFAP. Results and conclusion. Neurocognitive disorders with memory impairment in the long-term after severe traumatic brain injury are accompanied by a deepening of neurocyte degeneration and chronicity of neuroinflammation with activation of neuronal apoptosis and gliocyte autophagy mechanisms, which leads to irreversible deformation of the dentate gyrus cytoarchitectonics. The progression of neurodegeneration is accompanied by activation of microglia and leads to disintegration and migration of macrogliocytes with the formation of irreversible mosaic astrocytic deficiency and the formation of glial layers in the form of couplings around hemocapillaries. Preservation of memory function in animals with neurocognitive disorders is associated with the limitation of secondary neurocyte death and stabilization of adhesive properties of astroglia of the dentate cortex, which prevents the formation of astrocytic couplings around newly formed hemocapillaries while maintaining the integrity of the blood-brain barrier. In animals without neurocognitive disorders, compensatory mechanisms are implemented in the dentate cortex during long post-traumatic period through effective neovasculogenesis, limitation of perivascular astrocyte hyperplasia and neuroinflammation, which prevents neurocyte death and leads to the activation of synaptic remodeling from the entorhinal cortex to the CA1 area and from the dentate gyrus to the CA3 area of ​​the hippocampus 40 days after injury.