Increasing plasma thyroxine levels during late embryogenesis and hatching in the chicken are not caused by an increased sensitivity of the thyrotropes to hypothalamic stimulation.
The hatching process in the chicken is accompanied by dramatic changes in plasma thyroid hormones. The cause of these changes, though crucial for hatching and the onset of endothermy, is not known. One hypothesis is that the pituitary gland becomes more sensitive to hypothalamic stimulation during this period. We have tested whether the responsiveness of the thyrotropes to hypothalamic stimuli changes throughout the last week of embryonic development and hatching by studying the mRNA expression of receptors involved in the control of the secretory activity of this cell type. We used a real-time PCR set-up to quantify whole pituitary mRNA expression of the beta subunit of thyrotrophin (TSH-beta), type 1 thyrotrophin-releasing hormone receptor (TRH-R1), corticotrophin-releasing hormone receptors (CRH-R1 and CRH-R2) and somatostatin subtype receptor 2 (SSTR2) on every day of the last week of embryonic development, including the day of hatch and the first day of posthatch life. The thyrotrope-specific expression was investigated by a combination of in situ hybridization with immunohistochemistry at selected ages. Although TSH-beta mRNA levels increased towards day 19 of incubation (E19), the expression of CRH-R2 and TRH-R1 mRNA by the thyrotropes tended to decrease during this period, suggesting a lower sensitivity of the thyrotropes to the stimulatory factors CRH and TRH. CRH-R1, which is not involved in the control of TSH secretion, increased steadily throughout the period tested. The expression of SSTR2 mRNA by the thyrotropes was low during embryonic development and increased just before hatching. We have concluded that the sensitivity of the pituitary thyrotropes to hypothalamic stimulation decreases throughout the last week of embryonic development, so that the higher expression of TSH-beta mRNA around E16-E19, and hence the increasing plasma thyroxine level, is unlikely to be the result of an increased stimulation by either TRH or CRH.
De Groef
Bert
B
Laboratory of Comparative Endocrinology, K.U. Leuven, Naamsestraat 61, B3000 Leuven, Belgium. bert.degroef@bio.kuleuven.be
Grommen
Sylvia V H
SV
Darras
Veerle M
VM
D000818:Animals; D002642:Chick Embryo; D003345:Corticosterone / Q000097:blood; D047108:Embryonic Development / Q000502:physiology*; D007031:Hypothalamus / Q000196:embryology*; D007150:Immunohistochemistry / Q000379:methods; D017403:In Situ Hybridization / Q000379:methods; D010903:Pituitary Gland, Anterior / Q000166:cytology / Q000196:embryology*; D012333:RNA, Messenger / Q000032:analysis; D018019:Receptors, Corticotropin-Releasing Hormone / Q000032:analysis; D017481:Receptors, Somatostatin / Q000032:analysis; D018025:Receptors, Thyrotropin-Releasing Hormone / Q000032:analysis; D037322:Thyrotropin, beta Subunit / Q000032:analysis; D013974:Thyroxine / Q000097:blood*; D014284:Triiodothyronine / Q000097:blood
D012333:RNA, Messenger; D018019:Receptors, Corticotropin-Releasing Hormone; D017481:Receptors, Somatostatin; D018025:Receptors, Thyrotropin-Releasing Hormone; D037322:Thyrotropin, beta Subunit; D014284:Triiodothyronine; C093733:somatostatin receptor 2; D013974:Thyroxine; D003345:Corticosterone