Involvement of central prolactin-releasing peptide on stress-induced activation of hypothalamo-pituitary-adrenal axis in rats

Abstract

To confirm a role of prolactin-releasing peptide (PrRP) on stress response, we examined the effects of restraint stress (RTS), nociceptive stimulus and acute inflammatory stress in rats on the expression of the PrRP gene in the hypothalamus and medulla oblongata using in situ hybridization histochemistry. Moreover, we examined the effects of pretreatment with indomethacin on acute inflammation-induced PrRP gene expression and pretreatment with an anti-PrRP antibody on nociceptive stimulus-induced c-fos gene expression in the hypothalamic paraventricular nucleus (PVN). RTS, nociceptive stimulus and acute inflammatory stress upregulated the PrRP gene expression in the medulla oblongata. Acute inflammation-induced increase in the PrRP gene expression was significantly attenuated almost completely by prereatment with indomethacin. Pretreatment with anti-PrRP antibody attenuated significantly nociceptive stimulus-induced c-fos gene expression in the PVN. RTS, nociceptive stimulus and acute inflammatory stress activate PrRP neurons. Especially, activation of PrRP neurons by acute inflammation was mediated mainly by prostaglandins. Pretreatment with anti-PrRP antibody attenuated stress response via neurons in the PVN. These results suggested that PrRP is a potent and important mediator of stress response in the hypothalamic PVN in rats. [J Physiol Sci. 2006;56 Suppl:S218]