title: A role for neuropeptide Y in the gender-specific gastrointestinal, corticosterone and feeding responses to stress.
abstract: OBJECTIVE
  Exposure to an acute stress inhibits gastric emptying and stimulates colonic transit via central neuropeptide Y (NPY) pathways; however, peripheral involvement is uncertain. The anxiogenic phenotype of NPY(-/-) mice is gender-dependent, raising the possibility that stress-induced gastrointestinal (GI) responses are female-dominant through NPY. The aim of this study was to determine GI transit rates, corticosterone levels and food intake after acute restraint (AR) or novel environment (NE) stress in male and female NPY(-/-) and WT mice.
  
  
  METHODS
  Upper gastrointestinal transit (UGIT) (established 30 min after oral gavage) and corticosterone levels were determined under basal or restrained conditions (30 min) and after treatment i.p. with Y(1) antagonist BIBO3304 or Y(2) antagonist BIIE0246. Faecal pellet output (FPO) was established after AR and treatment i.p. with NPY in the NE, as were colonic bead expulsion rates.
  
  
  RESULTS
  UGIT and FPO were similar in unrestrained male and female mice. NPY(-/-) females displayed significantly slower UGIT than NPY(-/-) males after AR, but both genders displayed significantly higher FPO and reduced food intake relative to WT counterparts. Peripheral NPY treatment increased bead expulsion time in WT mice. AR male NPY(-/-) mice had higher levels of corticosterone than male WT mice; whilst in AR WT mice, after peripheral Y(1) and Y(2) receptor antagonism in males, and Y(2) antagonism in females, corticosterone was significantly elevated.
  
  
  CONCLUSIONS
  NPY possesses a role in the gender-dependent susceptibility to stress-induced GI responses. Furthermore, NPY inhibits GI motility through Y(2) receptors and corticosterone release via peripheral Y(1) and Y(2) receptors.
authors.affiliation: King's College London, Wolfson Centre for Age-Related Diseases, Guy's Campus, London, UK. sarah.forbes@kcl.ac.uk
authors.forename: S
authors.initials: S
authors.lastname: Forbes
authors.forename: H
authors.initials: H
authors.lastname: Herzog
authors.forename: H M
authors.initials: HM
authors.lastname: Cox
mesh_terms: D000818:Animals; D001120:Arginine / Q000031:analogs & derivatives* / Q000494:pharmacology; D001552:Benzazepines / Q000494:pharmacology*; D003345:Corticosterone / Q000097:blood*; D004435:Eating / Q000187:drug effects* / Q000502:physiology; D005260:Female; D005769:Gastrointestinal Motility / Q000187:drug effects; D041981:Gastrointestinal Tract / Q000187:drug effects* / Q000502:physiology; D008297:Male; D051379:Mice; D018345:Mice, Knockout; D009478:Neuropeptide Y / Q000819:agonists / Q000037:antagonists & inhibitors / Q000378:metabolism*; D012149:Restraint, Physical / Q000009:adverse effects; D012737:Sex Factors; D013312:Stress, Physiological / Q000502:physiology
chemical_list: D001552:Benzazepines; D009478:Neuropeptide Y; D001120:Arginine; C403256:BIIE 0246; C117416:BIBO 3304; D003345:Corticosterone