Post-stress changes in il-6 and bdnf mRNA levels in the hippocampus and blood of rats with a genetically determined contrast level of nervous system excitability

Abstract

Neuroinflammation is considered as one of the mechanisms by which stress can potentially lead to a disturbance of the functions of the central nervous system. The presence of neuroimmune dysfunction after stress, and what genetic factors increase the risk of post-stress neuroinflammation has not been sufficiently investigated. Genetically determined excitability of the nervous system is a promising marker of individual vulnerability to stress, manifested in post-stress disorders associated with the specifics of the formation of neuroinflammation.The aim of this work was to study post-stress changes in the expression of pro-inflammatory il-6 genes in the blood and hippocampus and anti-inflammatory cytokine bdnf in the blood of rats with genetically determined high and low levels of excitability of the nervous system. Breeding animals were used, males of two strains of rats aged 5 months: with a high threshold (HT) of excitability of the nervous system (low excitable) and a low threshold (LT) of excitability of the nervous system (high excitable) from the biological collection of the Pavlov Institute of Physiology of the Russian Academy of Sciences. The stress model is a long-term emotional and painful stress according to the scheme of K. Hecht. Experimental and control animals were decapitated 24 hours, 7 days and 24 days after the end of stress exposure. Changes in the mRNA level of the il-6 and bdnf genes were evaluated using real-time PCR.Chronic stress led to a significant increase in the level of il-6 mRNA in the hippocampus only in high excitable animals 24 days after the end of stress. In the blood, the mRNA level of this cytokine increased only in low-excitable rats. The expression of the bdnf gene in blood did not change in response to stress in any of the strains.