title: Possible inhibitory role of prolactin-releasing peptide for ACTH release associated with running stress.
abstract: Exercise around the lactate threshold induces a stress response, defined as "running stress." We have previously demonstrated that running stress is associated with activation of certain regions of the brain, e.g., the paraventricular hypothalamic nucleus (PVN) and supraoptic nucleus, that are hypothesized to play an integral role in regulating stress-related responses, including ACTH release during running. Thus we investigated the role of prolactin-releasing peptide (PrRP), found in the ventrolateral medulla and the nucleus of the solitary tract, which is known to project to the PVN during running-induced ACTH release. Accumulation of c-Fos in PrRP neurons correlated with running speeds, reaching maximal levels under running stress. Intracerebroventricular injection of neutralizing anti-PrRP antibodies led to increased plasma ACTH level and blood lactate accumulation during running stress, but not during restraint stress. Exogenous intracerebroventricular administration of low doses of PrRP had the opposite effects. Therefore, our results suggest that, during running stress, PrRP-containing neurons are activated in an exercise intensity-dependent manner, and likewise the produced endogenous PrRP attenuates ACTH release and blood lactate accumulation during running stress. Here we provide a novel perspective on understanding of PrRP in the endocrine-metabolic response associated with running stress.
authors.affiliation: Laboratory of Exercise Biochemistry, Graduate School of Comprehensive Human Sciences, University of Tsukuba, 1-1-1 Tennodai, Ibaraki, Japan.
authors.forename: Nao
authors.initials: N
authors.lastname: Ohiwa
authors.forename: Hyukki
authors.initials: H
authors.lastname: Chang
authors.forename: Tsuyoshi
authors.initials: T
authors.lastname: Saito
authors.forename: Tatsushi
authors.initials: T
authors.lastname: Onaka
authors.forename: Takahiko
authors.initials: T
authors.lastname: Fujikawa
authors.forename: Hideaki
authors.initials: H
authors.lastname: Soya
mesh_terms: D000324:Adrenocorticotropic Hormone / Q000378:metabolism*; D000818:Animals; D001786:Blood Glucose / Q000378:metabolism; D001923:Brain Chemistry / Q000502:physiology; D007028:Hypothalamic Hormones / Q000008:administration & dosage / Q000494:pharmacology / Q000502:physiology*; D007150:Immunohistochemistry; D007276:Injections, Intraventricular; D019344:Lactic Acid / Q000097:blood; D008297:Male; D009474:Neurons / Q000502:physiology; D009479:Neuropeptides / Q000008:administration & dosage / Q000494:pharmacology / Q000502:physiology*; D016761:Oncogene Proteins v-fos / Q000378:metabolism; D056690:Prolactin-Releasing Hormone; D051381:Rats; D017208:Rats, Wistar; D012149:Restraint, Physical; D012420:Running / Q000502:physiology*; D013312:Stress, Physiological / Q000378:metabolism*
chemical_list: D001786:Blood Glucose; D007028:Hypothalamic Hormones; D009479:Neuropeptides; D016761:Oncogene Proteins v-fos; C534377:PRLH protein, human; C534379:Prlh protein, rat; D056690:Prolactin-Releasing Hormone; D019344:Lactic Acid; D000324:Adrenocorticotropic Hormone