Morphofunctional Changes in Neurons, Glial Cells and Synapses in the Sensorimotor Cortex after Severe Traumatic Brain Injury

Abstract

The aim of the study was to investigate morphofunctional modifications in neurons, glial cells and synaptic terminals in the sensorimotor cortex of the brain in rats after severe traumatic brain injury (STBI).Material and methods. STBI simulation in white rats (main group, n=30) was performed on a device with a special shock mechanism. Intact animals (n=6) were included in the control group. The sensorimotor cortex (SMC) of the brain in rats was studied histomorphologically on sections stained with hematoxylin and eosin and thionin according to Nissl. Synaptophysin and GFAP were detected immunohistochemically, then morphometry was performed. On serial frontal sections of the SMC, neurons, neuroglia, and interneuronal synapses were studied in animals of the control group and in animals exposed to STBI in 1, 3, 7, 14, and 30 days after STBI simulation. The number density of neurons, neuroglia, and synaptic terminals was determined per a unit area of the section of layers I (terminals only), III, and V of the cerebral SMC. Statistical hypotheses were tested using nonparametric methods in the Statistica 10.0 program.Results. In animals of the control group, typical normochromic pyramidal neurons predominated, synaptic terminals were clearly verified; this was combined with unaltered neuropil. In animals exposed to STBI, there were signs of tinctorial, hydropic, dehydration and necrobiotic changes in neurons, reactive astrogliosis, fields of "loss" of neurons appeared; the overall numerical density of neurons and synapses decreased. The maximally increased content of pycnomorphic neurons was detected in 1 day after STBI (in layer III of the SMC, by 11.6%; in layer V of the SMC, by 18.5%). The peak in the number density of shadow cells and hyperchromic non-wrinkled neurons was noted in 3 days. The numerical density of synaptic terminals in different layers of the SMC decreased by 1.5-2 times. The altered balance of the destruction and restoration processes of the synaptic pool after STBI was evidenced by statistically significant data on the decreased and increased numerical density of terminals during 30 days of the study. There was no complete recovery of the studied parameters of neurons and synapses to control values within 30 days.Conclusion. The SMC of the brain in rats remains functioning after STBI; this occurs in the context of long-term preservation of reversibly and irreversibly damaged neurons, reactive neurogliosis, and permanent reorganization of interneuronal relationships due to activated reparative neuro- and synaptic plasticity. The data obtained will specify reorganization of the components of various neuronal complexes of the SMC (layers I, III, and V) after STBI.