Morphological bases of reorganization of the hippocampal interneuronal relationships in white rats after severe traumatic brain injury

Abstract

   The aim of the study was to investigate morphological changes in neurons, glia and synaptic terminals in cytoarchitectonic fields CA1 and CA3 of the hippocampus in white rats after severe traumatic brain injury (STBI).   Material and methods. This experimental study involved outbred adult white Wistar rats. STBI (main group, n = 30) was simulated under anesthesia (Zoletil-100) on the tailor-made device. Intact animals (n = 6) were used as controls. Morphological assessment of the hippocampal nervous tissue (in fields CA1 and CA3) was carried out using light microscopy (staining with hematoxylin and eosin, thionin according to Nissl), immunohistochemical reactions for synaptophysin (p38), Caspase 3, GFAP, and morphometric investigation techniques (ImageJ 1.53 program) in animals of the control group and in experimental animals in 1, 3, 7, 14, 30 days after STBI. Statistically hypotheses were tested using nonparametric tests (Kolmogorov–Smirnov, Kruskal–Wallis, Mann–Whitney, Wilcoxon, Spearman tests) in the Statistica program. 10.0.   Results. In a day after STBI, there were noted degeneratively altered dark neurons, shadow cells, small foci of neuron prolapse, pronounced manifestations of edema-swelling in the perikarya and neuropil. Coagulative-ischemic mechanisms of neuronal death prevailed, structural and immunohistochemical signs of apoptosis activation (Caspase 3 in the perikarya) were detected in sporadic cells of the field CA1. In the late period of the study (in 30 days), hydropic changes, chromatolysis with cytoplasmic clearing, hyperchromia without and with homogenization of neuronal structures persisted. An increased neuroglial index was distinctive. Statistically significant differences in the main morphometric parameters were revealed between segments and terms. The total number density of neurons decreased by 43.8 % in CA1 and in CA3 by 22.0 % in 30 days after injury; a significant (20–40 %) deficit of neuropil synapse terminals remained. Thus, the compensatory-restorative reorganization of the hippocampal neuronal networks occurred combined with its structural and functional insufficiency. Probably, Caspase 3 was crucial in implementing neuroplasticity.   Conclusion. Post-STBI diffuse-focal pathomorphological changes were revealed in CA1 and CA3 cells of the hippocampus. An increased relative content of glial cells indicated the realization of sanogenesis of the nervous tissue. Reorganization of interneuronal connections occurred during 30 days of observation, caspases might be participants of this process.