title: Prenatal and lactational bisphenol A exposure does not alter serotonergic neurons morphologically in the murine dorsal raphe nucleus.
abstract: OBJECTIVE
  There is concern that bisphenol A (BPA), an endocrine-disrupting chemical, affects brain development when exposed to a fetus and/or infant. We previously reported that increased serotonin (5-HT) and its metabolite (5-HIAA) in the dorsal raphe nucleus (DRN) in murine adult brains when they were prenatally exposed to low doses of BPA. This study investigates the morphological alteration of the dorsal raphe nucleus (DRN) in order to explain the disrupted serotonergic system after prenatal and lactational exposure to bisphenol A (BPA).
  
  
  METHODS
  The murine dams were orally administrated with 500μg/kg/day of BPA from embryonic day 0 to postnatal 3weeks. The DRN, the main region of serotonin production, was morphometrically analyzed at 14weeks, using immunohistochemistry and image analysis combined with 3-dimensional reconstruction.
  
  
  RESULTS
  No significant differences were revealed in the number of tryptophan hydroxylase 2-immunoreactive neurons in any of the DRN sub-regions or the morphometric parameters, including the whole volume, ventrodorsal, longitudinal, and wing lengths of the DRN among the BPA treatment and sex groups.
  
  
  CONCLUSIONS
  The murine DRN was not morphologically affected by prenatal and lactational exposure to low doses of BPA. Further studies are necessary regarding the function of serotonergic neurons and the activity of different kinds of related receptors in the brain.
authors.affiliation: Department of Pathology and Applied Neurobiology, Graduate School of Medical Science, Kyoto Prefectural University of Medicine, Japan; Department of Pathology, Meiji University of Integrative Medicine, Japan.
authors.forename: Shoko
authors.initials: S
authors.lastname: Goto
authors.affiliation: Department of Pathology and Applied Neurobiology, Graduate School of Medical Science, Kyoto Prefectural University of Medicine, Japan.
authors.forename: Hiroshi
authors.initials: H
authors.lastname: Ogi
authors.affiliation: Department of Pathology and Applied Neurobiology, Graduate School of Medical Science, Kyoto Prefectural University of Medicine, Japan.
authors.forename: Shinji
authors.initials: S
authors.lastname: Fushiki
authors.affiliation: Department of Pathology and Applied Neurobiology, Graduate School of Medical Science, Kyoto Prefectural University of Medicine, Japan. Electronic address: kxi14@koto.kpu-m.ac.jp.
authors.forename: Kyoko
authors.initials: K
authors.lastname: Itoh
mesh_terms: D000395:Air Pollutants, Occupational / Q000633:toxicity*; D000704:Analysis of Variance; D000818:Animals; D000831:Animals, Newborn; D001559:Benzhydryl Compounds / Q000633:toxicity*; D065847:Dorsal Raphe Nucleus / Q000000981:diagnostic imaging / Q000473:pathology*; D005260:Female; D005968:Glutamate Decarboxylase / Q000378:metabolism; D007774:Lactation / Q000187:drug effects*; D008297:Male; D051379:Mice; D008810:Mice, Inbred C57BL; D018613:Microscopy, Confocal; D010636:Phenols / Q000633:toxicity*; D011247:Pregnancy; D011297:Prenatal Exposure Delayed Effects / Q000139:chemically induced / Q000473:pathology / Q000503:physiopathology; D059326:Serotonergic Neurons / Q000187:drug effects* / Q000378:metabolism; D014365:Tryptophan Hydroxylase / Q000378:metabolism; D014446:Tyrosine 3-Monooxygenase / Q000378:metabolism; D000098826:Bisphenol A Compounds
chemical_list: D000395:Air Pollutants, Occupational; D001559:Benzhydryl Compounds; D005968:Glutamate Decarboxylase; D010636:Phenols; D014365:Tryptophan Hydroxylase; D014446:Tyrosine 3-Monooxygenase; C487802:Tph2 protein, mouse; C402565:glutamate decarboxylase 1; C006780:bisphenol A; D000098826:Bisphenol A Compounds
keywords: 3D-reconstruction; Development; Morphometry; Serotonin; Tryptophan hydroxylase 2