[Kainate receptors in the hippocampus of rat strains with different levels of the nervous system excitability].

Glutamate receptors in the central nervous system play a significant role in the mechanisms of differential adaptation to the environmental conditions. However, structural and functional parameters of kainate receptors (KR) under normal conditions and during exposure to stress are not well characterized. Therefore, the aim of this research was to 1) study the distribution and the quantity of KR GluR 5/6/7 subunits; 2) examine their changes in the pyramidal cell layer of the hippocampus in rat strains with have genetically determined distinctions in the levels of nervous system excitability following the exposure to short-term emotional-painful stress; 3) estimate the sensitivity of hippocampal pyramidal neurons to the action of KR agonist -kainic acid. It was demonstrated that GluR 5/6/7 KR are localized mainly in the region of hippocampal CA2 area; in the animals with low excitability their quantity was greater than in those with high excitability. Short-term emotional-painful stress resulted in the increase of KR in hippocampal CA2 area only in highly excitable rats. Selective sensitivity of pyramidal neurons in different hippocampal fields to the action of kainic acid was demonstrated and it was found to depend on animal strain characteristics of of the nervous system excitability.

[Systemic control of the molecular, cell, and epigenetic mechanisms of long-lasting consequences of stress].

Based on M.E. Lobashev's views of the systemic control of genetic and cytogeneitc processes and a substantial effect of excitability on plastic changes in the central nervous system (CNS), the effect of prolonged emotional and pain stress (PEPS) on the molecular, cell, and epigenetic mechanisms of injury memory was studied in rat strains bred for a certain excitability of the nervous system. PEPS was for the first time found to cause long-lasting (2 months) morphological alterations of the CA3 region of the hippocampus and to modify the genome activity of its pyramidal neurons. The two phenomena were potentiated by a genetically determined low functional state of the CNS. The post-stress regulation of the genome function in hippocampal neurons was mediated by changes in heterochromatin conformation, activation of methyl-CpG-binding protein (MeCP2) synthesis, and subsequent changes in acetylation of histone H4. Genetically determined high excitability of the nervous system proved to be a risk factor that affects the specifics and time course of the observed molecular, cell, and genetic transformations of neurons. The results provide for a better understanding of the epigenetic mechanisms of injury memory, which forms a pathogenetic basis for posttraumatic stress disorder and other human psychogenic conditions characterized by a prolonged duration.

[Heterochromatin characteristics in hippocampal neurons of rats with different excitability of the nervous system under conditions of posttraumatic stress disorder modeling].

Two lines of rats, selected according to the excitability of nervous system to the action of an electric current, served as the model objects to study the changes of heterochromatin characteristics in neurons of hippocampus (area CA3) 24 hours, 2 weeks, 2 and 6 months after exposure to prolonged emotional painful stress. It was shown that exposure to stress caused changes in the area, occupied by heterochromatin, only in rats with low-excitability: it was decreased 24 hours, 2 weeks and 2 months following the stress, while it was increased after 6 months as compared to control values. Thus, it was demonstrated for the first time that long-term modifications of heterochromatin structural characteristics of neurons in hippocampus (area CA3) could depend on genetically determined functional state of the nervous system.