Psychosocial stress inhibits additional stress-induced hyperexpression of NO synthases and IL-1β in brain structures

The aim of this study was to compare the expression of interleukin-1β (IL-1β), neuronal nitric oxide synthase (nNOS) and inducible nitric oxide synthase (iNOS) in the prefrontal cortex (PFC), hippocampus (HIP) and hypothalamus (HT) during chronic crowding (CS) (psychosocial) and restraint (RS) (physico-psychological) stress. Adaptational changes of these stress mediators to a subsequent acute RS, in two models of chronic stress were investigated.

Rats were crowded (24 in one cage) or restrained in metal tubes for 10min twice a day for 3, 7, and 14 consecutive days and decapitated. For determination of adaptational changes the chronically crowded and restrained rats 24h after the last stress session were subjected to a single 10min RS. The IL-1β, nNOS and iNOS protein levels in brain structures samples were analyzed by Western blot procedure.

Chronic CS for 3days did not markedly change the subsequent acute stress induced expression of nNOS, iNOS and IL-1β protein level in PFC and iNOS protein level in HT. CS markedly decreased the expression of nNOS, iNOS and IL-1β in HIP. By contrast, parallel chronic RS, significantly increased the subsequent acute stress-induced expression of iNOS and IL-1β in PFC and considerably increased iNOS level in HT.

Chronic psychosocial stress, may protect against possible harmful action of hyperproduction of iNOS and iNOS derived nitric oxide (NO) mainly in PFC and HIP. By contrast, chronic physico-psychosocial stress may strongly potentiate additional stress-induced harmful effects of NOS and IL-1β hyperproduction.