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Stress plays an important role in the pathogenesis of anxiety and depressive disorders. Neuroinflammation is considered as one of the mechanisms by which stress alters the molecular and cellular plasticity in the nervous tissue and thus entails CNS dysfunction. The contribution of genetically determined features of the nervous system to the development of post-stress neuroinflammation has not been sufficiently studied. In this study, the dynamics of post-stress changes in mRNA levels of the il-1 β and tnf genes encoding proinflammatory cytokines interleukin-1 beta (IL-1β) and tumor necrosis factor (TNF) were evaluated in the blood and brain of two rat strains with high and low excitability thresholds of the nervous system (HT and LT, respectively). Changes in IL-1β and TNF mRNA levels were assessed by real-time PCR 24 h, 7, 24 and 60 days after long-term long-term emotional and painful stress in the blood and three brain structures involved in the development of post-stress pathology (prefrontal cortex, hippocampus, amygdala). In highly excitable LT rats, IL-1β mRNA level in the hippocampus and amygdala increased compared to the control 24 days after stress termination, while in low-excitable HT animals, an increase in the level of IL-1β mRNA was only detected in the hippocampus at the same time point. TNF mRNA level did not change in any of the rat strains at any of the post-stress time points. Genetically determined excitability of the nervous system is a promising marker of individual stress vulnerability, as manifested in post-stress disorders associated with developmental and time-course features of neuroinflammation., Competing Interests: CONFLICT OF INTERESTThe authors declare that they have no conflict of interest., (© Pleiades Publishing, Ltd. 2023.)