Stress plays an important role in the pathogenesis of anxiety
and depressive disorders. Neuroinflammation is considered as one
of the mechanisms by which stress alters the molecular and cellular
plasticity in the nervous tissue and thus entails CNS dysfunction.
The contribution of genetically determined features of the nervous
system to the development of post-stress neuroinflammation has not
been sufficiently studied. In this study, the dynamics of post-stress changes
in mRNA levels of the
il-1
β
and
tnf
genes encoding proinflammatory
cytokines interleukin-1 beta (IL-1β) and tumor necrosis factor (TNF)
were evaluated in the blood and brain of two rat strains with high
and low excitability thresholds of the nervous system (HT and LT, respectively).
Changes in IL-1β and TNF mRNA levels were assessed by real-time
PCR 24 h, 7, 24 and 60 days after long-term long-term emotional
and painful stress in the blood and three brain structures involved
in the development of post-stress pathology (prefrontal cortex,
hippocampus, amygdala). In highly excitable LT rats, IL-1β mRNA
level in the hippocampus and amygdala increased compared to the
control 24 days after stress termination, while in low-excitable
HT animals, an increase in the level of IL-1β mRNA was only detected
in the hippocampus at the same time point. TNF mRNA level did not
change in any of the rat strains at any of the post-stress time points.
Genetically determined excitability of the nervous system is a promising
marker of individual stress vulnerability, as manifested in post-stress
disorders associated with developmental and time-course features
of neuroinflammation.