Adrenal inhibition of corticotropin-releasing hormone-induced thyrotropin release: A comparative study in pre- and posthatch chicks

Recent evidence indicates that corticotropin-releasing hormone (CRH) acts a sa potent stimulator of thyrotropin (TSH) release in the chicken. In this s tudy adrenal and thyroidal feedback mechanisms were studied. Administration of corticosterone 30 min prior to an ovine CRH (oCRH) challenge diminished the in vivo sensitivity of thyrotrophs to oCRH in 19-day-old chicken embry os (E19) (20 mu g corticosterone; 2 mu g oCRH) but not in 8-day-old chicken s (C8) (40 mu g corticosterone; 4 mu g oCRH). At both ages studied, cortico sterone (0.01 and 1 mu M) did not alter the in vitro TSH response to oCRH ( 100 nM) indicating that an indirect mechanism is involved at the embryonic stage which is no longer present in posthatch chickens. In vitro, 3,5,3'-triiodothyronine (T-3) pretreatment (0.01 and 1 mu M) resu lted at both ages studied in a dose-dependent drop in the in vitro oCRH-ind uced TSH release,As recorded previously, corticosterone treatment provoked a rise in plasma T-3 in embryonic but not in posthatch chickens. The presen ce of an indirect adrenal feedback mechanism in chicken embryos may therefo re be linked to the increase in plasma T-a which will alter the sensitivity of thyrotrophs to hypothalamic releasing factors. In conclusion, corticosterone does not directly modulate the responsiveness of thyrotrophs to CRH, but its feedback mechanism may be dependent on the evoked increase in plasma T-3 which is only present in embryonic chickens. Corticosterone may in this regard play an essential role during embryonic d evelopment by coordinating thyroidal feedback mechanisms at the level of th e chicken pituitary. (C) 1999 Wiley-Liss, Inc.