Post-stress pathological conditions are formed as a result of interaction of extreme environmental factors (including, psycho-emotional influences) and individual genomic features. The rats of two strains with high and low threshold of excitability of the nervous system (HT and LT) with a genetically determined predisposition to the development of disadaptive states under the influence of long-term emotional and painful stress (LEPS) are a unique model to explore genetic and epigenetic mechanisms of post-stress disorders (posttraumatic stress disorder and compulsive disorder, – PTSD, CD). The transcription activity of genome in brain neurons and chromosome aberrations level in the bone marrow cells of HT and LT rats under normal and stressor (LEPS) conditions was studied. Analysis of the percent of stained neurons of medial prefrontal cortex and basolateral amygdala with antibodies to acetylated H3 histone Lysine 9/14 (acH3K9/14) and to 5-methyl-cytosine (5 mc) revealed: 1) interlinear differences of the baseline level of acetylation of histone H3 and methylation of DNA; 2) the differential impact of LEPS (24 hours after procedure) on the transcriptional activity of the neurons of medial prefrontal cortex and basolateral amygdala in the rats of two strains (HT – an increase of acH3K9/14 and a decrease of 5 mc in both brain structures, LT– an increase of acH3K9/14 in amygdala only). The spontaneous chromosomal aberrations level in bone marrow cells revealed no interlinear differences. LEPS led to an increase in chromosomal aberrations level in mitosis, indicating the destabilization of chromosomes in rats of both lines, more significant in animals of the HT strain. The mechanisms of structural and regulatory changes in the genome in cells of central nervous system and peripheral organs under the influence of psychogenic stressors and their dependence on genetically determined features of nervous system excitability are discussed. The work was supported by the RFBR Grant № 16-04-00678