Regulation of CRH and AVP mRNA in the developing ovine hypothalamus: effects of stress and glucocorticoids

Abstract

Developmental changes in the abundance, localization, and distribution of corticotropin-releasing hormone (CRH) mRNA and arginine vasopressin (AVP) mRNA in the ovine hypothalamus were examined by in situ hybridization. The effects of fetal hypoxemia in the presence or absence of concomitant cortisol in late gestation (day 135) were also investigated. CRH and AVP mRNA were present at low levels within the paraventricular nucleus (PVN) and AVP mRNA was present in the supraoptic nucleus (SON) by day 60 (full term = 147 days). During late gestation, there were increases (P < 0.05, days 140–143 vs. days 100–120) in CRH mRNA, a further increase (P < 0.05, full term vs. days 140–143) at full term (fetuses delivered in active labor), and a subsequent decline postpartum (compared with full term). AVP mRNA in the magnocellular PVN increased (P < 0.05) in late gestation, levels did not change in parvocellular fields compared with full term fetuses, but magnocellular and parvocellular AVP mRNA increased in the newborn (P < 0.05, newborn vs. full term). AVP mRNA in the SON showed a developmental profile similar to that of the PVN, although there was an increase earlier in gestation (P < 0.05, days 100–120 vs. days 60–80). Hypoxemia caused increases (P < 0.05) in CRH mRNA, plasma adrenocorticotropic hormone, and cortisol concentrations, and although magnocellular and parvocellular AVP mRNA appeared elevated, changes just failed to attain significance. Cortisol infusion attenuated the hypoxemia-induced increase in CRH mRNA and adrenocorticotropic hormone but was without effect on basal CRH mRNA levels.