REGULATION OF CRH AND AVP MESSENGER-RNA IN THE DEVELOPING OVINE HYPOTHALAMUS - EFFECTS OF STRESS AND GLUCOCORTICOIDS

Citation
Sg. Matthews et Jrg. Challis, REGULATION OF CRH AND AVP MESSENGER-RNA IN THE DEVELOPING OVINE HYPOTHALAMUS - EFFECTS OF STRESS AND GLUCOCORTICOIDS, American journal of physiology: endocrinology and metabolism, 31(6), 1995, pp. 1096-1107
Citations number
38
Categorie Soggetti
Physiology
ISSN journal
01931849
Volume
31
Issue
6
Year of publication
1995
Pages
1096 - 1107
Database
ISI
SICI code
0193-1849(1995)31:6<1096:ROCAAM>2.0.ZU;2-P
Abstract
Developmental changes in the abundance, localization, and distribution of corticotropin-releasing hormone (CRH) mRNA and arginine vasopressi n (AVP) mRNA in the ovine hypothalamus were examined by in situ hybrid ization. The effects of fetal hyperemia in the presence or absence of concomitant cortisol in late gestation (day 135) were also investigate d. CRH and AVP mRNA were present at low levels within the paraventricu lar nucleus (PVN) and AVP mRNA was present in the supraoptic nucleus ( SON) by day 60 (full term = 147 days). During late gestation, there we re 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 postpartu m (compared with full term). AVP mRNA in the magnocellular PVN increas ed (P < 0.05) in late gestation, levels did not change in parvocellula r fields compared with full term fetuses, but magnocellular and parvoc ellular AVP mRNA increased in the newborn (P < 0.05, newborn vs. full term). AVP mRNA in the SON showed a developmental profile similar to t hat 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 c oncentrations, and although magnocellular and parvocellular AVP mRNA a ppeared elevated, changes just failed to attain significance. Cortisol infusion attenuated the hypoxemia-induced increase in CRH mRNA and ad renocorticotropic hormone but was without effect on basal CRH mRNA lev els.