Corticosterone- or metapyrone-induced alterations in adrenal function and expression of the arginine vasotocin receptor VT2 in the pituitary gland of domestic fowl, Gallus gallus.

Abstract:

:The avian neurohypophyseal hormone arginine vasotocin (AVT) is known to be involved in the regulation of adrenocorticotropin (ACTH) release by interacting with the VT2 receptor (VT2R), which is homologous to the mammalian vasopressin V1b receptor (V1bR). To study the role of glucocorticoid in the expression and regulation of the VT2R, corticosterone (1 or 5mg/bird/day) or metapyrone (10 or 50mg/kg body weight/day) were administered daily for 8 days to white leghorn chickens. While low doses were ineffective, a high dose of corticosterone upregulated, while metapyrone downregulated, pituitary VT2R mRNA expression and ir-VT2 in the cephalic lobe of the anterior pituitary. Further, although no change was observed in the expression of POMC mRNA, adrenal activity (as judged by the changes in total cholesterol, 3beta HSD, cortical cord width and cortico-medullary ratio) exhibited suppression or stimulation following treatment with corticosterone or metapyrone, respectively. In view of the classical negative feedback effect of glucocorticoids at the level of hypothalamic CRH neurons and pituitary corticotrophs, high corticosterone level-induced suppression of the CRH-ACTH axis may have been masked by VT2R-mediated stimulation of corticotrophs, and hence the POMC mRNA level did not change. The same argument could be used for metapyrone. It is concluded that expression of the VT2 receptor is regulated by glucocorticoids in chicken. These findings confirm a role for AVT, mediated by the VT2 receptor, in regulating ACTH secretion during stress and suggest that corticotroph VT2 receptor levels may be dynamically regulated depending on the HPA axis activity.

journal_name

Gen Comp Endocrinol

authors

Sharma D,Cornett LE,Chaturvedi CM

doi

10.1016/j.ygcen.2008.12.019

subject

Has Abstract

pub_date

2009-04-01 00:00:00

pages

208-15

issue

2

eissn

0016-6480

issn

1095-6840

pii

S0016-6480(09)00005-7

journal_volume

161

pub_type

杂志文章