title: Hypothalamic-pituitary-adrenal axis function in pony foals after neonatal ACTH-induced glucocorticoid overexposure.
abstract: BACKGROUND
  The effects of overexposure to glucocorticoids during early life of the foal on the subsequent HPA programming of the hypothalamic-pituitary-adrenal axis are unknown.
  
  
  OBJECTIVE
  To test the hypotheses that excess glucocorticoid exposure in early life subsequently increases both basal plasma concentrations of cortisol and the adrenocortical responsiveness to exogenous adrenocorticotropic hormone (ACTH).
  
  
  METHODS
  Foals received either saline (0.9% NaCl, n = 9) or long-acting ACTH (0.125 mg i.m. b.i.d., n = 6) for 5 days from Day 1 to increase endogenous cortisol concentrations. Long-term indwelling catheters were inserted under local anaesthesia into the jugular veins of foals aged 2 and 12 weeks. After recovery, short-acting ACTH1-24 was given as a single i.v. injection (2 microg/kg bwt) and blood samples were taken at 5-30 min intervals before and after ACTH administration to measure plasma cortisol concentrations.
  
  
  RESULTS
  Basal plasma cortisol concentrations were higher in ACTH- than in saline-treated foals at age 3 weeks, but not at 13 weeks. There were no significant differences in either the time profile or the area under the cortisol curve in response to ACTH between the 2 groups.
  
  
  CONCLUSIONS
  These data suggest that ACTH-induced overexposure to glucocorticoids during early post natal life of the foal does not have a programming effect on HPA axis function at 13 weeks. In foals, the effects of ACTH-induced overexposure to glucocorticoids, if any, may not become apparent until much later in life in a long-lived species such as the horse.
  
  
  CONCLUSIONS
  These studies suggest that clinical and other stressful conditions that raise plasma cortisol concentrations during early life are unlikely to programme cardiovascular and metabolic function in horses in the short term.
authors.affiliation: Department of Physiology, Development and Neuroscience, University of Cambridge, UK. J.K.Jellyman.00@cantab.net
authors.forename: J K
authors.initials: JK
authors.lastname: Jellyman
authors.forename: V L
authors.initials: VL
authors.lastname: Allen
authors.forename: A J
authors.initials: AJ
authors.lastname: Forhead
authors.forename: N B
authors.initials: NB
authors.lastname: Holdstock
authors.forename: A L
authors.initials: AL
authors.lastname: Fowden
mesh_terms: D000311:Adrenal Glands / Q000187:drug effects / Q000502:physiology; D000818:Animals; D000831:Animals, Newborn; D003366:Cosyntropin / Q000494:pharmacology*; D005260:Female; D006736:Horses / Q000502:physiology*; D006854:Hydrocortisone / Q000097:blood; D007030:Hypothalamo-Hypophyseal System / Q000187:drug effects* / Q000502:physiology; D008297:Male; D010913:Pituitary-Adrenal System / Q000187:drug effects* / Q000502:physiology
chemical_list: D003366:Cosyntropin; C006418:adrenocorticotropin zinc; D006854:Hydrocortisone