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.