title: Opioids are responsible for neurochemical feminization of the brain in prenatally stressed male rats.
abstract: OBJECTIVE
  To study the role of opioids in early postnatal changes of the hypothalamic testosterone metabolism and catecholamine content underlying feminizing effect of prenatal stress on male sexual behavior in rats.
  
  
  METHODS
  10 day-old male and female offspring from mothers given naltrexone prior to daily 1-hour restraint during the last gestational week were used in the study. Aromatase and 5 alpha-reductase activities, noradrenaline and dopamine contents in the brain preoptic area and medial basal hypothalamus were studied by thin layer chromatography, radiometric and spectrofluorimetric techniques.
  
  
  RESULTS
  Sexual dimorphism of testosterone metabolism enzymes activity and catecholamine content in discrete brain regions of 10 day-old rat pups was found. Prenatal stress attenuated these gender-related differences. Naltrexone pre-treatment of stressed dams prevented modifying effect of prenatal stress on aromatase activity and noradrenaline content in the male preoptic area.
  
  
  CONCLUSIONS
  The results of the study demonstrate preventive effect of naltrexone on stress-induced alterations of testosterone aromatization and noradrenaline concentration in the developing brain preoptic area associated with neuroendocrine control of the male sexual behavior in adult rats. These findings indicate that endogenic opioids mediate detrimental effect of prenatal stress on neurochemical determinants of the brain sexual differentiation that may underlie feminization of the male sexual behavior.
authors.affiliation: Department of Endocrinology of Reproduction and Adaptation, Institute of Endocrinology and Metabolism, Kiev, Ukraine. dccie@mail.kar.net
authors.forename: Alexander G
authors.initials: AG
authors.lastname: Reznikov
authors.forename: Nadezhda D
authors.initials: ND
authors.lastname: Nosenko
authors.forename: Larisa V
authors.initials: LV
authors.lastname: Tarasenko
mesh_terms: D013741:3-Oxo-5-alpha-Steroid 4-Dehydrogenase / Q000378:metabolism; D000818:Animals; D001141:Aromatase / Q000378:metabolism; D001923:Brain Chemistry / Q000502:physiology*; D002395:Catecholamines / Q000378:metabolism; D002855:Chromatography, Thin Layer; D004298:Dopamine / Q000378:metabolism; D005260:Female; D005262:Feminization / Q000503:physiopathology*; D007031:Hypothalamus / Q000378:metabolism; D008297:Male; D009271:Naltrexone / Q000494:pharmacology; D009292:Narcotic Antagonists / Q000494:pharmacology; D009638:Norepinephrine / Q000378:metabolism; D018847:Opioid Peptides / Q000502:physiology*; D011247:Pregnancy; D011297:Prenatal Exposure Delayed Effects; D011301:Preoptic Area / Q000378:metabolism; D051381:Rats; D012727:Sex Characteristics; D013050:Spectrometry, Fluorescence; D013315:Stress, Psychological / Q000503:physiopathology*; D013739:Testosterone / Q000378:metabolism
chemical_list: D002395:Catecholamines; D009292:Narcotic Antagonists; D018847:Opioid Peptides; D013739:Testosterone; D009271:Naltrexone; D001141:Aromatase; D013741:3-Oxo-5-alpha-Steroid 4-Dehydrogenase; D004298:Dopamine; D009638:Norepinephrine