De Groef Bert, Grommen Sylvia V H, Darras Veerle M
Laboratory of Comparative Endocrinology, Catholic University of Leuven, Naamsestraat 61, B3000 Leuven, Belgium.
Gen Comp Endocrinol. 2007 Jun-Jul;152(2-3):178-82. doi: 10.1016/j.ygcen.2007.01.036. Epub 2007 Feb 9.
We have studied the involvement of the somatostatin receptor type 5 (SSTR5) in the control of thyrotropin (TSH) release in the chicken. Hypothalamic somatostatin (SS-14) is known to inhibit both thyrotropin-releasing hormone (TRH)- and corticotropin-releasing hormone (CRH)-induced TSH secretion. Studies using receptor-specific agonists have indicated that the inhibitory effect of SS-14 on TRH-induced TSH release is mediated by SSTR2 and SSTR5. Using the same agonists, we were able to demonstrate the involvement of SSTR5 in the inhibition of the in vitro CRH-induced TSH secretion by SS-14. Subsequently, we determined hypophyseal SSTR5 mRNA expression during the last week of embryonic development using real-time PCR. SSTR5 mRNA levels were low until day 19 of incubation, but between day 19 and hatching SSTR5 mRNA expression increased 3-fold. Since this increase coincides with the increasing plasma T(3) levels towards hatching, and a similar ontogenetic expression pattern was found for SSTR2, we quantified hypophyseal SSTR2 and SSTR5 mRNA expression levels in chicken embryos treated with thyroid hormones. Injection of thyroid hormones was indeed found to increase the expression of both mRNAs significantly. We hypothesize that the negative feedback exerted by the increasing plasma T(3) levels towards hatching is at least in part mediated by an increased expression of SSTR2 and SSTR5.
