title: Prenatal dexamethasone exposure alters brain monoamine metabolism and adrenocortical response in rat offspring.
abstract: In this study, it has been clearly demonstrated that prenatal dexamethasone treatment (Dex; 0.05 mg/kg on gestational days 17, 18, and 19) resulted in the significant reductions of 5-hydroxytryptamine (5-HT) turnover in four brain regions, including the neocortex, hippocampus, hypothalamus, and midbrain + pons-medulla (M + P-M) but not in the striatum in the offspring at 3 and 14 wk of life, as well as dopamine turnover in the hypothalamus. [3H]paroxetine binding densities were increased in the hypothalamus and M + P-M at 14 wk of life, which corresponded to increased 5-HT contents in both regions. On the other hand, significantly lower norepinephrine contents in the neocortex and hippocampus were observed in the Dex group compared with the control group at 14 wk of life. In addition, the exposure to new environmental condition elevated blood corticosterone levels and enhanced behavioral activities to a greater extent in the Dex group than in controls at 7 wk of life, suggesting that elevated glucocorticoid levels during the pregnancy mimicked prenatal mild stress, producing developmental alterations in brain monoamine metabolism, endocrine response, and behavior in adult offspring.
authors.affiliation: Department of Neuropsychiatry, Kagoshima University Faculty of Medicine, Japan.
authors.forename: K
authors.initials: K
authors.lastname: Muneoka
authors.forename: M
authors.initials: M
authors.lastname: Mikuni
authors.forename: T
authors.initials: T
authors.lastname: Ogawa
authors.forename: K
authors.initials: K
authors.lastname: Kitera
authors.forename: K
authors.initials: K
authors.lastname: Kamei
authors.forename: M
authors.initials: M
authors.lastname: Takigawa
authors.forename: K
authors.initials: K
authors.lastname: Takahashi
mesh_terms: D015102:3,4-Dihydroxyphenylacetic Acid / Q000378:metabolism; D000302:Adrenal Cortex / Q000187:drug effects / Q000254:growth & development / Q000502:physiology*; D000375:Aging / Q000502:physiology*; D000704:Analysis of Variance; D000818:Animals; D015306:Biogenic Monoamines / Q000378:metabolism*; D001921:Brain / Q000187:drug effects / Q000254:growth & development / Q000378:metabolism*; D003345:Corticosterone / Q000097:blood; D003672:Defecation; D003907:Dexamethasone / Q000494:pharmacology*; D004298:Dopamine / Q000378:metabolism; D005260:Female; D005865:Gestational Age; D006719:Homovanillic Acid / Q000378:metabolism; D006897:Hydroxyindoleacetic Acid / Q000378:metabolism; D008297:Male; D009043:Motor Activity / Q000187:drug effects; D009928:Organ Specificity; D017374:Paroxetine / Q000378:metabolism; D011247:Pregnancy; D011297:Prenatal Exposure Delayed Effects; D051381:Rats; D017207:Rats, Sprague-Dawley; D012701:Serotonin / Q000378:metabolism*
chemical_list: D015306:Biogenic Monoamines; D015102:3,4-Dihydroxyphenylacetic Acid; D012701:Serotonin; D017374:Paroxetine; D006897:Hydroxyindoleacetic Acid; D003907:Dexamethasone; D004298:Dopamine; D003345:Corticosterone; D006719:Homovanillic Acid