Effects of psychogenic stress on some peripheral and central inflammatory markers in rats with the different level of excitability of the nervous system

Abstract

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.

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

“…A higher blood level of il 1β mRNA expression was detected in highly excitable LT rats compared to low excitable HT animals. This is consistent with our previous data that highly excitable rats develop signs of inflammation in the blood in response to chronic stress, as manifested in changes in the leukocyte formula [13].…”

“…The obtained results are in good agreement with the data avail able in the literature that in the CNS, unlike at the periphery, high GC doses or long term stress lead to an increased production of inflammatory mediators and microglia activation [7,17]. We have previously shown [13] that the number of microglial cells increases 7 days after stress expo sure in the dentate gyrus (DG), hippocampal CA1 and CA3 fields in LT rats and in the CA1 field in HT animals, which does not contemporize with the increase in the level of il 1β gene expression observed in the present work, as it occurs only on day 24 against a normalization of the number of microglial cell. Activation and proliferation of microglia, as well as blood-brain monocyte traf ficking, being the main sources of IL 1β and TNF, occur after some latent period, and this may account for the delay described above.…”

“…It has been shown that the strains differ by their behavioral responses, molecular and cellular changes in nervous tissue during the development of poststress states. Rats with low excitability (high threshold, HT strain) exhibit delayed depressive-like behavioral symptoms in response to long-term emotional and painful stress exposure, while rats with high excitability (low threshold, LT strain) develop compulsive symptoms along with the depressive-like [ 13 ].…”

“…We have previously shown that the level of nervous system’s excitability also influences the degree of manifestation and dynamics of poststress inflammation both in the blood and in the brain in response to long-term emotional and painful stress. The neutrophil/leukocyte ratio and microglia cell count in the hippocampus increase in highly excitable animals compared to controls [ 13 ]. It is important to clarify the molecular mechanisms of neuroinflammation at the level of il-1 β and tnf gene expression of the major proinflammatory cytokines, interleukin-1β (IL-1β) and tumor necrosis factor (TNF).…”

Single Prolonged Stress Decreases the Level of Adult Hippocampal Neurogenesis in C57BL/6, but Not in House Mice

“…The number of Iba+ cells in the dentate gyrus also did not change after stress, but house mice had significantly more microglia than C57BL/6 animals. In our previous study with two rat strains with different levels of excitability of the nervous system [51], we have shown that animals of the highly excitable strain had significantly less Iba+ cells in the hippocampus than the less excitable strain [52]. Highly excitable rats seemed to be more susceptible to immune dysfunctions in response to chronic stress.…”