title: Effects of glucocorticoid on brain acetylcholinesterase of developing chick embryos.
abstract: OBJECTIVE
  Fetal exposure to excessive or deficient glucocorticoids may alter the programming in differentiation and maturation of various tissues including the brain and nervous system, leading to dysfunctions later in life. For further exploration of this possibility, we established an animal model using developing chick embryos.
  
  
  METHODS
  (i) Reverse-transcription polymerase chain reaction was used to determine the expression of glucocorticoid receptor mRNA in the brain of chick embryos. (ii) Embryos on day 15 were administered betamethasone or mifepristone and their cerebrum, cerebellum and optic lobe were investigated to determine the activity of acetylcholinesterase.
  
  
  RESULTS
  (i) Glucocorticoid receptor mRNA was shown to be present in the cerebrum, cerebellum and optic lobe. (ii) After the administration of betamethasone, acetylcholinesterase activities in the cerebrum, cerebellum and optic lobe on day 19 were 1.5- to 2-fold higher than those of untreated control. Weights of body and brain parts were 0.65-0.75-fold relative to control values. However, these differences were less noticeable on day 22. (iii) Administration of mifepristone before treatment with betamethasone prevented high-dose betamethasone-induced changes in acetylcholinesterase activity and bodyweights on day 19. Administration of mifepristone alone did not induce differences from the control.
  
  
  CONCLUSIONS
  The cerebrum, cerebellum and optic lobe of chick embryos could be influenced by glucocorticoids because of the presence of glucocorticoid receptor mRNA. Although the effects observed after treatment with excess glucocorticoids (even no effects after mifepristone treatment) were transitory, they may alter the developmental program in ways that could result in lasting change and influence behavioral activities after hatching.
authors.affiliation: Department of Obstetrics and Gynecology, School of Medicine, Iwate Medical University, Iwate, Japan.
authors.forename: Sumire
authors.initials: S
authors.lastname: Yamate
authors.forename: Hidekazu
authors.initials: H
authors.lastname: Nishigori
authors.forename: Seishi
authors.initials: S
authors.lastname: Kishimoto
authors.forename: Yu
authors.initials: Y
authors.lastname: Tezuka
authors.forename: Akimune
authors.initials: A
authors.lastname: Fukushima
authors.forename: Toru
authors.initials: T
authors.lastname: Sugiyama
authors.forename: Hideo
authors.initials: H
authors.lastname: Nishigori
mesh_terms: D000110:Acetylcholinesterase / Q000378:metabolism*; D000818:Animals; D001623:Betamethasone / Q000008:administration & dosage / Q000494:pharmacology*; D001921:Brain / Q000187:drug effects* / Q000196:embryology / Q000378:metabolism; D002642:Chick Embryo; D005938:Glucocorticoids / Q000008:administration & dosage / Q000494:pharmacology*; D006727:Hormone Antagonists / Q000494:pharmacology; D015735:Mifepristone / Q000494:pharmacology; D011965:Receptors, Glucocorticoid / Q000037:antagonists & inhibitors / Q000235:genetics / Q000378:metabolism
chemical_list: D005938:Glucocorticoids; D006727:Hormone Antagonists; D011965:Receptors, Glucocorticoid; D015735:Mifepristone; D001623:Betamethasone; D000110:Acetylcholinesterase