title: Prenatal and neonatal exposure to bisphenol-A enhances the central dopamine D1 receptor-mediated action in mice: enhancement of the methamphetamine-induced abuse state.
abstract: Bisphenol-A (BPA), one of the most common environmental endocrine disrupters, has been extensively evaluated for toxicity in a variety of tests in rodents, including developmental and reproductive toxicity, and carcinogenicity. However, little is known about its action on the CNS. In this report, we show that prenatal and neonatal exposure to BPA in mice leads to the enhancement of the dopamine D1 receptor-dependent rewarding effect induced by a psychostimulant methamphetamine. Furthermore, this treatment with BPA markedly enhanced hyperlocomotion and its sensitization induced by methamphetamine, which reflects extensive abuse associated with sociological and psychiatric problems. We also demonstrated that chronic exposure to BPA produced an up-regulation of dopamine D1 receptor function to activate G-protein in the mouse limbic forebrain, which is thought to be a critical site for the expression of rewarding effects by abuse drugs. Additionally, chronic BPA exposure produced a significant increase in levels of the dopamine D1 receptor mRNA in the whole brain. In contrast, no change in protein levels of methamphetamine-targeted proteins, dopamine transporter or the type 2 vesicle monoamine transporter in the brain was observed by prenatal and neonatal exposure to BPA. The present data provide the first evidence that prenatal and neonatal exposure to BPA can potentiate the central dopamine D1 receptor-dependent neurotransmission, resulting in supersensitivity of methamphetamine-induced pharmacological actions related to psychological dependence on psychostimulants.
authors.affiliation: Department of Toxicology, School of Pharmacy and Pharmaceutical Sciences, 2-4-41 Ebara, Shinagawa-ku, Tokyo 142-8501, Japan. suzuki@hoshi.ac.jp
authors.forename: T
authors.initials: T
authors.lastname: Suzuki
authors.forename: K
authors.initials: K
authors.lastname: Mizuo
authors.forename: H
authors.initials: H
authors.lastname: Nakazawa
authors.forename: Y
authors.initials: Y
authors.lastname: Funae
authors.forename: S
authors.initials: S
authors.lastname: Fushiki
authors.forename: S
authors.initials: S
authors.lastname: Fukushima
authors.forename: T
authors.initials: T
authors.lastname: Shirai
authors.forename: M
authors.initials: M
authors.lastname: Narita
mesh_terms: D000395:Air Pollutants, Occupational / Q000633:toxicity*; D019969:Amphetamine-Related Disorders / Q000378:metabolism*; D000818:Animals; D000831:Animals, Newborn; D001522:Behavior, Animal / Q000187:drug effects; D001552:Benzazepines / Q000494:pharmacology; D001559:Benzhydryl Compounds; D015153:Blotting, Western; D001921:Brain / Q000187:drug effects / Q000378:metabolism; D000697:Central Nervous System Stimulants / Q000494:pharmacology*; D003213:Conditioning, Psychological / Q000187:drug effects; D018492:Dopamine Antagonists / Q000494:pharmacology; D004305:Dose-Response Relationship, Drug; D004357:Drug Synergism; D005260:Female; D019204:GTP-Binding Proteins / Q000378:metabolism; D008124:Locomotion / Q000187:drug effects; D008694:Methamphetamine / Q000494:pharmacology*; D051379:Mice; D010636:Phenols / Q000633:toxicity*; D011247:Pregnancy; D011297:Prenatal Exposure Delayed Effects; D012333:RNA, Messenger / Q000096:biosynthesis; D011869:Radioligand Assay; D011930:Reaction Time; D017447:Receptors, Dopamine D1 / Q000187:drug effects / Q000378:metabolism*; D020133:Reverse Transcriptase Polymerase Chain Reaction; D013469:Sulpiride / Q000494:pharmacology; D000098826:Bisphenol A Compounds
chemical_list: D000395:Air Pollutants, Occupational; D001552:Benzazepines; D001559:Benzhydryl Compounds; D000697:Central Nervous System Stimulants; D018492:Dopamine Antagonists; D019204:GTP-Binding Proteins; D008694:Methamphetamine; D010636:Phenols; D012333:RNA, Messenger; D017447:Receptors, Dopamine D1; D013469:Sulpiride; C006780:bisphenol A; D000098826:Bisphenol A Compounds