Ovarian and extraovarian sources of immunoreactive inhibin in the chicken: effects of dexamethasone.
Academic Article
Overview
Research
Identity
Additional Document Info
Other
View All
Overview
abstract
The present study investigates whether besides the ovary, extragonadal sources contribute to the total amount of immunoreactive inhibin in the plasma of the domestic hen. A comparison of the inhibin content of different organ shows that, expressed per milligram of tissue, the adrenal ranks second only to the ovarian granulosa layer. To explore the contribution of the adrenals to plasma inhibin, dexamethasone (100 micrograms/kg BW) was injected i.v. into intact, ovariectomized, and sham-operated hens. Control animals of each experimental group were injected with saline (0.9% (w/v) NaCI). Dexamethasone significantly (P < 0.05) decreased plasma inhibin concentrations in the three groups. The suppressive effect of dexamethasone in intact hens, however, was caused by a direct effect of this synthetic glucocorticoid on the gonads. Indeed, dexamethasone decreased the production of inhibin by granulosa cells in vitro and also lowered the immunoreactive inhibin concentration in ovariectomized animals. The decreased plasma inhibin concentration in ovariectomized animals is probably due to a direct effect of dexamethasone on the adrenals. Adrenal cells produced immunoreactive inhibin in vitro. The inhibin secretion by adrenal cells was significantly (P < 0.05) depressed by dexamethasone. In conclusion, the ovary is the major source of plasma immunoreactive inhibin in the laying hen. The presence of substantial amounts of immunoreactive inhibin in the adrenal, the secretion of inhibin by cultured adrenal cells, and the decreased immunoreactive inhibin in ovariectomized animals treated with dexamethasone indicate that the adrenal is a likely source of extragonadal inhibin. The nature and the role of this adrenal inhibin remain to be investigated.