Somatotropin response in vitro to corticosterone and triiodothyronine during chick embryonic development: Involvement of type I and type II glucocorticoid receptors

Abstract

Corticosterone (CORT) can stimulate growth hormone (GH) secretion on embryonic day (e) 12 in the chicken. However, CORT failed to induce GH secretion on e20 in a single report, suggesting that regulation of GH production changes during embryonic development. Secretion in response to CORT during embryonic development is modulated by the thyroid hormones triiodothyronine (T 3) and thyroxine (T 4). Growth hormone responses on e12 involve both glucocorticoid (GR) and mineralocorticoid receptors (MR); however, involvement of MR has not been evaluated past e12. To further define changes in somatotroph responsiveness to CORT, pituitary cells obtained on e12–e20 were cultured with CORT alone and in combination with T 3 and GH-releasing hormone (GHRH). Growth hormone mRNA levels and protein secretion were quantified by quantitative real-time polymerase chain reaction (qRT-PCR) and radioimmunoassay (RIA), respectively. Corticosterone significantly increased GH mRNA and protein secretion on e12; however, mRNA concentration and protein secretion were unaffected on e20. Contributions of GR and MR in CORT responses were evaluated using GR and MR antagonists. Treatment with a GR-specific antagonist effectively blocked the CORT-induced increase in GH secretion on e12. The same treatment on e20 had no effect on GH secretion. These findings demonstrate that GR is directly involved in glucocorticoid stimulation of GH secretion at the time of somatotroph differentiation but is not regulatory at the end of embryonic development. We conclude that positive somatotroph responses to CORT are lost during chicken embryonic development and that GR is the primary regulator of CORT-induced GH secretion.