title: Prolactin induces phosphorylation of the STAT5 in adrenal glands of Hatano rats during stress.
abstract: OBJECTIVE
  To investigate the signaling of prolactin (PRL) in the adrenal gland during stress in Hatano high- (HAA) and low-avoidance (LAA) rats.
  
  
  METHODS
  Adrenal glands of both strains were collected at 0, 15 and 30 min after stress. The protein levels of phosphorylated STAT5 and the mRNA levels of melanocortin receptor 2 (MC2R) and PRL receptor (PRLR) were analyzed. Furthermore, the effects of bromocriptine-induced hypoprolactinemia on adrenocortical responses to stress were investigated.
  
  
  RESULTS
  Adrenocorticotropic hormone (ACTH) concentrations in HAA were greater than LAA, while the difference in PRL concentrations were found only at 120 min after stress induction. No strain differences were observed in corticosterone or progesterone in response to stress. The stress-induced increase in MC2R mRNA expression was higher in HAA, but there was a lowered PRLR mRNA expression. STAT5 become highly phosphorylated in response to stress in both strains, but bromocriptine led to a reduction the STAT5 phosphorylation. Exposure to bromocriptine was associated with a reduction in plasma PRL in response to stress in both strains, while the ACTH levels were not altered. However, the decrease in corticosterone and progesterone in response to stress was observed only in bromocriptine-treated LAA rats.
  
  
  CONCLUSIONS
  These data show that PRL plays an important role in the regulation of corticosterone and progesterone release in LAA but not in HAA during stress. These results suggest that PRL increase in response to stress, and it acts on the adrenal cortex and thereby plays an important physiologic role in protecting against acute stress.
authors.affiliation: Department of Basic Veterinary Science, The United School of Veterinary Sciences, Gifu University, Gifu 501-1193, Japan.
authors.forename: Sukanya
authors.initials: S
authors.lastname: Jaroenporn
authors.forename: Kentaro
authors.initials: K
authors.lastname: Nagaoka
authors.forename: Ryo
authors.initials: R
authors.lastname: Ohta
authors.forename: Gen
authors.initials: G
authors.lastname: Watanabe
authors.forename: Kazuyoshi
authors.initials: K
authors.lastname: Taya
mesh_terms: D000311:Adrenal Glands / Q000187:drug effects / Q000378:metabolism*; D000324:Adrenocorticotropic Hormone / Q000378:metabolism; D000818:Animals; D001971:Bromocriptine / Q000494:pharmacology; D006727:Hormone Antagonists / Q000494:pharmacology; D008297:Male; D010766:Phosphorylation / Q000187:drug effects; D011388:Prolactin / Q000097:blood / Q000502:physiology*; D051381:Rats; D011919:Rats, Inbred Strains; D044103:Receptor, Melanocortin, Type 2 / Q000096:biosynthesis; D011981:Receptors, Prolactin / Q000096:biosynthesis; D050799:STAT5 Transcription Factor / Q000378:metabolism*; D013312:Stress, Physiological / Q000187:drug effects
chemical_list: D006727:Hormone Antagonists; D044103:Receptor, Melanocortin, Type 2; D011981:Receptors, Prolactin; D050799:STAT5 Transcription Factor; D001971:Bromocriptine; D000324:Adrenocorticotropic Hormone; D011388:Prolactin