Stress-induced expression of immediate early genes in the brain and peripheral organs of the rat

Stress causes rapid and transient expression of immediate early genes (IEGs) in the brain, and the monitoring of IEGs has enabled the visualization of the neurocircuitry of stress. Previous studies have postulated that stressors can be divided into two categories; processive and systemic. The neural circuits of brain activation differ between the two kinds of stressors. For example, processive stressors, such as immobilization (IMO), induce c-fos mRNA first in the cortical and limbic areas and then in the paraventricular hypothalamic nucleus (PVH), while c-fos expression in the PVH precedes that in other areas in animals subjected to systemic stressors. We further show that prior exposure to IMO stress for 6 days, or implantation of corticosterone pellets suppresses the induction of c-fos, fos B, jun B and NGFI-B, but not that of NGFI-A in the rat PVH. Plasma glucocorticoid may be an important factor regulating stress-induced IEG expression. It is well known that AP-1 and glucocorticoid receptors (GR) interact and suppress each other. Thus, decreased AP-1 levels in chronically stressed animals may help enhance the negative feedback effects of GR and prevent hypersecretion of glucocorticoid, which is implicated in the pathogenesis of stress-related diseases. IMO stress induces rapid expression of c-fos, c-jun and NGFI-A mRNAs in the heart and stomach. These were observed in the ventricular myocardium and coronary arteries, and in the epithelium, smooth muscles and arteries of the stomach after 30 min of IMO. IEG expression in the peripheral organs may provide a molecular basis for stress-induced psychosomatic disorders.