Abstract
Prolactin-releasing peptide (PrRP) is known to play a role in the function of the hypothalamic-pituitary-adrenal axis. To analyze the function of PrRP as a stress mediator, we studied the effects of acute inflammation and nociceptive stimulus on the PrRP gene expression in the rat brain, using in situ hybridization histochemistry. Adult male rats (200-250 g) were used in all experiments. As an acute inflammatory stress, rats were intraperitoneally (ip) injected with lipopolysaccharide (LPS) from E. coli at a dose of 5 mg/kg body weight. LPS was dissolved in pyrogen-free 0.9% saline with 1 mg/ml. Control rats were ip injected with 1 ml of pyrogen-free 0.9% saline. All rats were decapitated at 3, 6, 12, 24 and 48 hr after ip injection. As a nociceptive stress, rats were subcutaneously (sc) injected with 100μl of 5% formalin in 0.9% saline into the dorsal surface of each hind paw. Control rats were sc injected with 100μl of 0.9% saline. All rats were decapitated at 3, 6, 12 and 24 hr after sc injection. After an acute inflammatory stress, PrRP mRNA levels in the nucleus tractus solitarius (NTS) and the ventrolateral medulla (VLM) were significantly increased. After a nociceptive stress, PrRP mRNA levels in the VLM were significantly increased. These results suggest that acute inflammation and nociceptive stimulus may be potent stimulants to up-regulate the PrRP gene expression in the rat brain. [Jpn J Physiol 55 Suppl:S211 (2005)]
