Testosterone modulates pituitary vasotocin receptor expression and adrenal activity in osmotically stressed chicken

Regulation of arginine vasotocin (AVT), avian neurohypophyseal hormone, is an important component of the hypothalamo-pituitary–adrenal axis. Changes in plasma osmolality levels and sex steroids are known to affect AVT gene expression. The present study reports the effect of water deprivation and testosterone treatment independently, as well as simultaneously, on the pituitary vasotocin receptor VT2R expression and adrenal steroidogenic activity in sexually immature male chicken (Gallus gallus). Birds were divided into four groups— control, water deprived (WD), testosterone injected (TE) and TE treated water deprived (TE+WD). WD decreased and TE treatment alone or in combination with WD (TE+WD) increased VT2R expression compared to the control. Expression of pro-opiomelanocortin (POMC) was also studied since this gene is a polypeptide precursor of ACTH and is under the negative feedback of adrenal corticoids. TE treatment as well as WD separately or when coupled together decreased the POMC mRNA expression in the pituitary but stimulated adrenal steroidogenic activity. Further, VT2R expression decreased in TE+WD compared to TE group, but it was not different from the vehicle treated control group suggesting that the suppressive effect of WD on VT2R expression was inhibited by the stimulatory effect of testosterone. Similarly, although both TE and WD decreased POMC expression and increased steroidogenic activity, no further decrease or increase in these parameters was observed when these two (WD and TE) treatments were combined together. Although, the exact mechanism is not clear, data indicate a stimulatory action of testosterone on VT2R expression and adrenal function despite a decreased expression of POMC mRNA. Results also suggest that testosterone treatment to sexually immature birds, in addition to its effect on hypothalamic AVT neurons (earlier study) and pituitary VT2R expression (present study), masks or inhibits osmotic stress-induced alterations in pituitary–adrenal activity.