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 asa potent stimulator of thyrotropin (TSH) release in the chicken. In this study 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 embryos (E19) (20 mu g corticosterone; 2 mu g oCRH) but not in 8-day-old chickens (C8) (40 mu g corticosterone; 4 mu g oCRH). At both ages studied, corticosterone (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) resulted at both ages studied in a dose-dependent drop in the in vitro oCRH-induced TSH release,As recorded previously, corticosterone treatment provoked a rise in plasma T-3 in embryonic but not in posthatch chickens. The presence of an indirect adrenal feedback mechanism in chicken embryos may therefore 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 development by coordinating thyroidal feedback mechanisms at the level of the chicken pituitary. (C) 1999 Wiley-Liss, Inc.