Dynamics of structural rearrangements in the entorhinal cortex in rats with various neurocognitive disorders after traumatic brain injury

Damage to brain tissue and transformation of the microvascular bed after traumatic brain injury determine a wide range of changes in neurons and neuroglial cells, but the dependence of these changes on the localization of damage requires further clarification. The study aims to study the tissue and cellular posttraumatic changes in the structure of the brain entorhinal cortex in rats with various neurocognitive disorders at different times after severe traumatic brain injury. 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: the first – animals after trauma with neurocognitive disorders and memory disorders; the second – animals after trauma with neurocognitive disorders without memory disorders; the third comparison group – animals after trauma without neurocognitive disorders. A histological, morphometric and immunohistochemical study of the brain parahippocampal gyrus of the frontal lobe was carried out using the markers β-tubulin, Synaptophysin, GAP43, NCAM1, N-cadherin, GFAP. Statistical processing of the obtained results was carried out in the licensed software package “Statistica v6.1” using parametric and nonparametric methods. The morphological substrate of neurocognitive disorders with memory impairment in the long-term after injury in rats is the irreversible deformation of the cytoarchitectonics of the parahippocampal gyrus and the deepening of the degeneration of neurocytes of the entorhinal cortex due to the blocking of transendothelial transport by astrocytic conglomerates with the destruction of the blood-brain barrier. The progression of neurodegeneration is accompanied by the activation of microglia and leads to the disintegration and migration of macrogliocytes with the formation of an irreversible mosaic astrocytic deficiency, as well as to the formation of glial deposits in the form of couplings around hemocapillaries. The safeguarding of memory function in animals with neurocognitive disorders is carried out by limiting the secondary death of neurocytes and stabilizing the adhesive properties of astroglia of the entorhinal cortex. 10 days after injury, there is an increase in NCAM1 expression with the initiation of cell adhesion, which after 20 days of the experiment leads to axon regeneration and renovation of synaptic activity. This is accompanied by an increase in GAP43 expression by preserved neurocytes with remodeling of presynaptic terminals and restoration of afferentation from the entorhinal cortex to the hippocampal CA1 area 40 days after injury. Thus, compensation for the metabolic and excitotoxic consequences of brain injury is realized through effective neovasculogenesis, limitation of perivascular astrocyte hyperplasia and neuroinflammation, which prevents neurocyte death and leads to activation of synaptic remodeling by GAP43-positive neurons.