Physical and inflammatory stressors elevate circadian clock gene mPer1 mRNA levels in the paraventricular nucleus of the mouse

Stress induces secretion of corticosterone through activation of hypothalam ic-pituitary-adrenal axis. This corticosterone the hy secretion is thought to be controlled by a circadian clock in the suprachiasmatic nucleus (SCN). The hypothalamic paraventricular nucleus (PVN) receives convergent informa tion from both stress and the circadian clock. Recent reports demonstrate t hat mammalian orthologs (Per1, Per2, and Per3) of the Drosophila clock gene Period are expressed in the SCN, PVN, and peripheral tissues. In this expe riment, we examined the effect of physical and inflammatory stressors on mP er gene expression in the SCN, PVN, and liver. Forced swimming, immobilizat ion, and lipopolysaccharide injection elevated mPer1 gene expression in the PVN but not in the SCN or liver. A stress-induced increase in mPer1 expres sion was observed in the corticotropin-releasing factor-positive cells of t he PVN; however, the stressors used in this study did not affect mPer2 expr ession in the PVN, SCN, or liver. The present study suggests that a stress- induced disturbance of circadian corticosterone secretion may be associated with the stress-induced expression of mPer1 mRNA in the PVN.