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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.

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A model system consisting of two rat strains bred for nervous system excitability in response to electric shocks was used to study changes in the number density of neurons in hippocampal field CA3 at 24 h, two weeks, and two and six months after prolonged emotional-pain stress (PEPS). Neuron density in hippocampal field CA3 decreased after completion of PEPS. These changes arose at different time points in the different rat strains (one day for low-excitability rats, two months for high-excitability rats) and persisted to six months. Thus, this is the first demonstration that persistent differential effects of stress on the number density of neurons in hippocampal field CA3, which plays an important role in learning and memory processes, depend on genetically determined constitutive characteristics of the nervous system.

An enhancement of stress reactivity of the hypophysial-adrenocortical system in response to emotional and physical influence was shown in rats with a low threshold of sensitivity to electrical current. This phenomenon was observed as a rise in the maximum level of blood corticosterone and acceleration of stressor hormonal response. In the high-threshold rats a decrease in sensitivity of the hypophysial adrenocortical system to the feedback signals was observed. Key Words: hypophysial adrenocortical system; stress reactivity; corticosterone; line ratsAnimal experiments confirm that basic properties of the nervous system are determined genetically [6]. Selection according to the excitability threshold of the nerve-muscle apparatus [2] show that not only behavioral characteristics, but also reactivity to stress and ability to adapt to the environment depend on the excitability of the nervous system [1,9,10]. These findings support the hypothesis that the divergence of these properties is determined predominantly by hypophysial-adrenocortical system (HACS). There are data indicating that neuron excitability depends on corticosteroids [13]. We studied functional state of HACS in rats, in which not only the peripheral subdivision of nervous system [2], but also its central structures, the midbrain reticular formation in particular [5], had different threshold of excitability [2]. MATERIALS AND METHODSThe study was carried out on 120 male Wistar rats weighing 350+_.25 g, which were genetieaUy selected according to the threshold of sensitivity of the tibial I.P. Pavlov Institute of Physiology, Russian Academy of Sciences, St. Petersburg nerve to electrical current. Selection was performed from two independent autobred populations: the high sensitivity LT-1 and LT-2 rats (low threshold: first selection program --34th generation and the second selection program --24th generation) and low sensitivity HTol and HT-2 rats (high threshold: the first and second selection programs of the same generations). The rats were grown and maintained on the standard diet at the Laboratory of Genetics of Highest Nervous System (I.P. Pavlov Institute of Physiology).Basal state of HACS was evaluated by plasma content of cortieosterone (CS) at rest. Blood samples were taken from the caudal vein at 4 p.m. Stress response of HACS was estimated by the maximum rise in blood CS. Several types of stressor stimulation were used. Emotional stress caused by new environment was estimated by measuring blood CS after a 30 rain vein (I series). In the 2nd series, the rats were stimulated transeutaneously with electrical current (0.5 rnA, 50 Hz, maximum duration 15 see) which was applied 15 times to the floor of a 20x20x 13 em chamber. Blood was taken from the caudal vein 1, 3, and 24 h after stimulation.The sensitivity of HACS to feedback signals was determined in a 2-day dexamethasone test [4].Two

Priority data on specific effect of long-term mental and pain stress on the dynamics of H4 histone acetylation in the pyramidal neuron nuclei of the hippocampal CA3 field in rats selected by the nervous system excitability were obtained using a comparative genetic method. The congruency of long-term post-stress modification of H4 histone acetylation in neurons of rats with high threshold excitability and behavioral changes intrinsic of these rats suggest that increased acetylation of H4 histone together with changes in heterochromatin conformation play a triggering role in long-term modifications of genome expression underlying the pathogenesis of posttraumatic stress disorders and other psychogenias.

Stress during pregnancy affects the morphogenesis of embryonal brain, its structural and functional characteristics, and behavior of the progeny. Genetic mechanisms of this process remain unclear. Cytogenetic characteristics of neuroblasts were analyzed in 17-18-day embryos of rats selected by threshold excitability of the nervous system in health and after emotional painful stress during the third trimester of pregnancy. The strains differed by the effect of stress on proliferative activity and chromosome aberrations in cells of the future hippocampus depending on the strain-specific characteristics of the nervous system excitability. This effect is regarded as an important component of epigenetic regulation of neurogenesis and behavior.

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