Involvement of thyrotropin-releasing hormone receptor, somatostatin receptor subtype 2 and corticotropin-releasing hormone receptor type 1 in the control of chicken thyrotropin secretion.

Thyrotropin or thyroid-stimulating hormone (TSH) secretion in the chicken is controlled by several hypothalamic hormones. It is stimulated by thyrotropin-releasing hormone (TRH) and corticotropin-releasing hormone (CRH), whereas somatostatin (SRIH) exerts an inhibitory effect. In order to determine the mechanism by which these hypothalamic hormones modulate chicken TSH release, we examined the cellular localization of TRH receptors (TRH-R), CRH receptors type 1 (CRH-R1) and somatostatin subtype 2 receptors (SSTR2) in the chicken pars distalis by in situ hybridization (ISH), combined with immunological staining of thyrotropes. We show that thyrotropes express TRH-Rs and SSTR2s, allowing a direct action of TRH and SRIH at the level of the thyrotropes. CRH-R1 expression is virtually confined to corticotropes, suggesting that CRH-induced adrenocorticotropin release is the result of a direct stimulation of corticotropes, whereas CRH-stimulated TSH release is not directly mediated by the known chicken CRH-R1. Possibly CRH-induced TSH secretion is mediated by a yet unknown type of CRH-R in the chicken. Alternatively, a pro-opiomelanocortin (POMC)-derived peptide, secreted by the corticotropes following CRH stimulation, could act as an activator of TSH secretion in a paracrine way.

Evidence of a thyrotropin-releasing activity of ovine corticotropin-releasing factor in the domestic fowl (Gallus domesticus).

Ovine corticotropin-releasing factor (oCRF) administered to 19-day-old chicken embryos (E19) increased plasma concentration of pituitary glycoprotein alpha-subunit concentrations within 15 min for at least 4 hr. Follicle stimulating hormone levels were unchanged, while plasma luteinizing hormone concentrations only began to increase 1 hr after the oCRF treatment. Calculation of circulating thyrotropin (TSH) indicator values revealed a rapid elevation in TSH plasma levels following oCRF. Concentrations of thyroxine (T4), 3,5,3'-triiodothyronine (T3), 3,3',5'-triiodothyronine (rT3), and corticosterone increased from 1 hr postinjection. Hypothalamic outer ring deiodinating type II increased and hepatic inner ring deiodinating type III fell after 2 and 4 hr, explaining at least in part the plasma T3 increase at the end of the experiment. In a second experiment, using E18 chicks, a comparison was made between the effects of a single injection of 2 micrograms oCRF and 20 mlU bovine TSH. Both hormones increased T4, T3, and rT3 plasma concentrations, supporting the hypothesis of a TSH-releasing activity for oCRF in the embryonic chicken. The proposed TSH-mediated effect of CRF on thyroid function was further confirmed in two in vitro experiments in which oCRF did not directly influence the thyroidal T4 secretion but, when applied to pituitaries, clearly increased the alpha-subunit release. In chickens CRF is concluded to not only control the adrenal axis, but also to participate in the coordination of avian TSH release.