title: Chronic ethanol exposure increases the non-dominant glucocorticoid, corticosterone, in the near-term pregnant guinea pig.
abstract: Maternal-fetal signaling is critical for optimal fetal development and postnatal outcomes. Chronic ethanol exposure alters programming of the fetal hypothalamic-pituitary-adrenal (HPA) axis, resulting in a myriad of neurochemical and behavioral alterations in postnatal life. Based on a recent study which showed that human intra-partum fetal stress increased fetal secretion of corticosterone, the non-dominant glucocorticoid, this investigation tested the hypothesis that an established model of HPA axis programming, chronic maternal ethanol administration to the pregnant guinea pig, would result in preferential elevation of corticosterone, which is also the non-dominant glucocorticoid. Starting on gestational day (GD) 2, guinea pigs received oral administration of ethanol (4 g/kg maternal body weight/day) or isocaloric-sucrose/pair-feeding. Each treatment was administered daily and continued until GD 45, 55, or 65 (approximately 3 days pre-term), when pregnant animals were euthanized and fetuses delivered by Caesarean section. Maternal and fetal plasma samples were collected. After sample preparation (protein precipitation and C-18 solid phase extraction), plasma cortisol and corticosterone concentrations were determined simultaneously by liquid chromatography coupled to tandem mass spectrometry. As predicted, chronic ethanol exposure increased both fetal and maternal plasma corticosterone concentration in late gestation. In contrast, plasma cortisol did not differ across maternal treatments in maternal or fetal samples. The plasma concentration of both maternal glucocorticoids increased with gestational age. Thus, corticosterone, the non-dominant glucocorticoid, but not cortisol, was elevated by chronic ethanol exposure, which may have effects on HPA function in later life.
authors: Department of Biomedical and Molecular Sciences, Queen's University, Kingston, ON, Canada K7L 3N6.
authors: Amy J
authors: AJ
authors: Hewitt
authors: Department of Biomedical and Molecular Sciences, Queen's University, Kingston, ON, Canada K7L 3N6.
authors: Christine C
authors: CC
authors: Dobson
authors: Department of Biomedical and Molecular Sciences, Queen's University, Kingston, ON, Canada K7L 3N6; Centre for Neuroscience Studies, Queen's University, Kingston, ON, Canada K7L 3N6.
authors: James F
authors: JF
authors: Brien
authors: Department of Comparative Biology and Experimental Medicine, Faculty of Veterinary Medicine, and Hotchkiss Brain Institute, University of Calgary, Calgary, AB, Canada T2N 4N1.
authors: Katherine E
authors: KE
authors: Wynne-Edwards
authors: Department of Biomedical and Molecular Sciences, Queen's University, Kingston, ON, Canada K7L 3N6; Centre for Neuroscience Studies, Queen's University, Kingston, ON, Canada K7L 3N6. Electronic address: jnr@queensu.ca.
authors: James N
authors: JN
authors: Reynolds
mesh_terms: D000818:Animals; D003345:Corticosterone / Q000097:blood*; D000431:Ethanol / Q000008:administration & dosage*; D005260:Female; D005312:Fetal Blood / Q000737:chemistry; D047109:Fetal Development / Q000187:drug effects; D006168:Guinea Pigs; D006854:Hydrocortisone / Q000097:blood; D007030:Hypothalamo-Hypophyseal System / Q000187:drug effects; D010913:Pituitary-Adrenal System / Q000187:drug effects; D011247:Pregnancy; D011270:Pregnancy, Animal / Q000187:drug effects*
chemical_list: D000431:Ethanol; D003345:Corticosterone; D006854:Hydrocortisone
keywords: Chronic ethanol exposure; Corticosterone; Cortisol; Maternal-fetal stress