Patients with post-stress pathologies display the signs of inflammation in the peripheral blood as well as in the brain. The mechanisms of such post-stress neuroimmune changes, their contribution to the behavior, the relationship of the intensity of inflammation with genetically determined features have not been clarified. The goal of this work was to evaluate the dynamics of post-stress inflammation in the blood and hippocampus of rats which differ in level of excitability of the nervous system. Rats of two strains (high/low excitability threshold) were subjected to stress according to the K. Hecht protocol and their behavior, neutrophil:lymphocyte ratio and the number of Iba+ cells in the hippocampus were analysed 24 hours, 7 and 24 days after stress exposure. Highly excitable animals show an increase in anxiety-like behavior, in the number of neutrophils compared to lymphocytes as well as in the number of Iba1+ cells in CA1, CA3 and DG areas of the hippocampus in response to stress. Thus, hereditary high excitability of the nervous system is a possible risk factor for the development of post-stress pathologies.

We studied changes in the stability of the genome in cells of two brain regions (prefrontal cortex and hippocampus), as well as in the bone marrow of rats with a hereditary high and low thresholds of excitability of the nervous system (strains HT and LT, respectively) after prolonged exposure with emotional-pain stressor. To study the reactivity of the brain cells genome, phosphorylated histone -H2AX (-H2AX phospho Ser139) was used. The level of mitotic disturbances in bone marrow cells was also assessed. Between the animals of the control groups, there were no interstrain differences in the studied parameters. Stress exposure increases the immunoreactivity to -H2AX phospho Ser139 of the prefrontal cortex cells and the level of chromosomal aberrations in bone marrow cells in animals of both strains. In cells of the dentate gyrus of the hippocampus, a specific increase in immunoreactivity to -H2AX phospho Ser139 was revealed in rats of the low-excitable HT strain. The relationship between the reaction of cells of this zone of hippocampus to the stressor exposure with the hereditary level of excitability of the nervous system of animals is discussed.

No abstract

Post-stress states in animals and humans are accompanied by the development of neuro- and peripheral inflammation. The mechanisms of such immune dysfunctions, their contribution to the pathogenesis of stress-related diseases, as well as the dependence of the intensity of poststress inflammation on genetically determined features of the nervous system, have not been clarified.Aim: to assess the dynamics of the development of poststress inflammation depending on the genetically determined level of excitability of the nervous system in rats.Materials and methods. The study was carried out on male rats of two lines, selected by the threshold of excitability of the nervous system-the line HT (high threshold of excitability) and LT (low threshold of excitability). As a model of chronic stress, the Protocol of long-term emotional and pain exposure according to Hecht was used. To investigate the dynamics of changes in the leukocyte formula, three time points were selected: 24 hours, 7 days and 24 days after the stressor. Morphological analysis of blood was carried out to determine the leukogram, for which the leukocytes were counted in a blood smear stained by Romanovsky-Gimza.Results. Chronic stress leads to an increase in the leukocyte shift index only in the experimental group of highly excitable rats of the LT line compared with control animals of the same line. The significance of the differences is confirmed on day 7 after the end of the stressor. No interline differences in neutrophil/lymphocyte ratios were found in intact animals of LT and HT lines.Conclusion. In rats with a genetically determined high level of excitability of the nervous system, post-stressor systemic inflammation appears 7 days after the end of the stressor. Animals with a low level of excitability of the nervous system had no signs of post-stress inflammation throughout the observations. The article discusses the possible mechanisms of detected immune dysfunctions in animals due to high excitability of the central nervous system.

Changes of genome stability in hippocampal cells of male rats with hereditary high and low thresholds of nervus tibialis response to electric stimuli (HT and LT strains, respectively) were studied in unstressed and stressed animals. HT and LT originated from Wistar strain, males of which were also used as a control. The comet assay was used after prolonged emotional painful stressor action. There were no interstrain differences in the spontaneous percentage of DNA in comet tails (tDNA). However, the prolonged emotional pain stressor induced genome instability differently in animals of different strains. The highest level of DNA damage in hippocampal cells was shown in highly sensitive animals of LT strain. Males of Wistar strain had intermediate levels of tDNA, while HT animals had the lowest stress reactivity.