title: Abnormalities of hypothalamic-pituitary-adrenal and hypothalamic-somatotrophic axes in Fawn-Hooded rats.
abstract: Fawn-Hooded (FH) rats show central and peripheral abnormalities in serotoninergic functions and have attracted attention as an animal model of some pathologies, including depression and hypertension. In addition, these rats show a reduced growth rate. As the hypothalamic-pituitary-adrenal (HPA) axis has been implicated in both depression and hypertension, and the hypothalamic-somatotrophic (HSM) axis has a major role in growth, these two endocrine axes were characterised in FH rats as compared with outbred Sprague-Dawley (SD) rats in basal conditions. FH rats showed normal serum ACTH and corticosterone concentrations, but reduced serum corticosterone binding capacity. At a central level, normal expression of mRNA for glucocorticoid type II receptors in the hippocampal formation and mRNA for corticotrophin-releasing factor (CRF) in the paraventricular nucleus of the hypothalamus were observed in FH rats, whereas expression of mRNA for CRF in the central nucleus of the amygdala was enhanced compared with the expression in SD rats. Serum GH concentrations were normal in FH rats, IGF-I tended to be lower, and mRNA for somatostatin (SRIF) in the periventricular nucleus of the hypothalamus was significantly lower in FH rats than in SD rats. The reduced SRIF gene expression in rats with normal or slightly reduced GH and IGF-I, respectively, might be secondary to a defective central and peripheral response to IGF-I, compatible with the reduced growth of FH rats. The present results suggest that FH rats have abnormalities in both HPA and HSM axes that might be related to some of their physiopathological characteristics.
authors.affiliation: Unitat de Fisiologia Animal, Departament de Biologia Cellular, de Fisiologia i d'Immunologie, Facultat de Cièncias, Universitat Autónoma de Barcelona, 08193 Bellaterra, Barcelona, Spain.
authors.forename: F
authors.initials: F
authors.lastname: Gómez
authors.forename: P
authors.initials: P
authors.lastname: Graugés
authors.forename: A
authors.initials: A
authors.lastname: López-Calderón
authors.forename: A
authors.initials: A
authors.lastname: Armario
mesh_terms: D000324:Adrenocorticotropic Hormone / Q000097:blood; D000818:Animals; D001921:Brain / Q000503:physiopathology*; D003345:Corticosterone / Q000097:blood; D003346:Corticotropin-Releasing Hormone / Q000302:isolation & purification; D015342:DNA Probes / Q000737:chemistry; D004195:Disease Models, Animal; D005786:Gene Expression Regulation; D013006:Growth Hormone / Q000097:blood / Q000302:isolation & purification; D007030:Hypothalamo-Hypophyseal System / Q000503:physiopathology*; D015592:Immunoradiometric Assay / Q000662:veterinary; D017403:In Situ Hybridization / Q000662:veterinary; D007334:Insulin-Like Growth Factor I / Q000032:analysis; D008297:Male; D010913:Pituitary-Adrenal System / Q000503:physiopathology*; D011863:Radioimmunoassay / Q000662:veterinary; D051381:Rats; D017207:Rats, Sprague-Dawley; D011965:Receptors, Glucocorticoid / Q000302:isolation & purification; D012701:Serotonin / Q000502:physiology*; D014156:Transcortin / Q000502:physiology
chemical_list: D015342:DNA Probes; D011965:Receptors, Glucocorticoid; D012701:Serotonin; D007334:Insulin-Like Growth Factor I; D000324:Adrenocorticotropic Hormone; D013006:Growth Hormone; D014156:Transcortin; D003346:Corticotropin-Releasing Hormone; D003345:Corticosterone