The Effect of Long-Term Emotional and Painful Stress on the Expression of Proinflammatory Cytokine Genes in Rats with High and Low Excitability of the Nervous System

Abstract

Stress plays an important role in the pathogenesis of anxietyand depressive disorders. Neuroinflammation is considered as oneof the mechanisms by which stress alters the molecular and cellularplasticity in the nervous tissue and thus entails CNS dysfunction.The contribution of genetically determined features of the nervoussystem to the development of post-stress neuroinflammation has notbeen sufficiently studied. In this study, the dynamics of post-stress changesin mRNA levels of the il-1βand tnf genes encoding proinflammatorycytokines interleukin-1 beta (IL-1β) and tumor necrosis factor (TNF)were evaluated in the blood and brain of two rat strains with highand low excitability thresholds of the nervous system (HT and LT, respectively).Changes in IL-1β and TNF mRNA levels were assessed by real-timePCR 24 h, 7, 24 and 60 days after long-term long-term emotionaland painful stress in the blood and three brain structures involvedin the development of post-stress pathology (prefrontal cortex,hippocampus, amygdala). In highly excitable LT rats, IL-1β mRNAlevel in the hippocampus and amygdala increased compared to thecontrol 24 days after stress termination, while in low-excitableHT animals, an increase in the level of IL-1β mRNA was only detectedin the hippocampus at the same time point. TNF mRNA level did notchange in any of the rat strains at any of the post-stress time points.Genetically determined excitability of the nervous system is a promisingmarker of individual stress vulnerability, as manifested in post-stressdisorders associated with developmental and time-course featuresof neuroinflammation.