Prenatal Corticosterone Exposure Alters Glucocorticoid Metabolic Enzyme Eene mRNA Associated with Increased Aggressive Behaviors and Tonic Immobility in Chicken

Exposure to excess Glucocorticoids (GCs) during embryonic development influences offspring physiology and behaviors and induces change in Hypothalamic-Pituitary-Adrenal (HPA) axis genes expression and serotonergic system in mammals. Whether prenatal corticosterone (CORT) exposure induces similar effects in avian species remains unclear. In the present study, we injected low (0.2 μg) and high (1 μg) doses of CORT in ovo before incubation and detected changes in aggressive behavior, Tonic Immobility (TI), HPA axis and 5-hydroxytryptamine (serotonin) (5-HT) system gene expression on post hatch chickens of different ages. High dose of CORT significantly (P<0.05) suppressed growth rate, increased the frequency of aggressive behaviors, which was associated with elevated plasma CORT concentration. Likewise, in ovo injection of CORT significantly (P<0.05) increased Tonic Immobility (TI) duration both in chickens from low and high doses of CORT treatments compared to control. In addition, administration of CORT significantly (P<0.05) up-regulated mRNA expression of 11β-hydroxysteroid dehydrogenase type 1 (11β-HSD1) whereas it down-regulated 11β-hydroxysteroid dehydrogenase type 2 (11β-HSD2) and mineralocorticoid receptor (MR) mRNA expression in the hypothalamus. No significant differences were seen in Glucocorticoid Receptor (GR) and 20-hydroxysteroid dehydrogenase (20-HSD) mRNA levels upon CORT treatment. Moreover, CORT exposure significantly (P<0.05) increased hypothalamic 5-hydroxytryptamine (serotonin) receptor 1A (5-HTR1A) mRNA expression, but not 5-HT receptor 1B (5-HTR1B). In ovo administration of CORT may programs the aggressive behaviors in the chicken through alterations of HPA axis and 5-HT system.