| Literature DB >> 9473372 |
D A Larsen1, P Swanson, J T Dickey, J Rivier, W W Dickhoff.
Abstract
Investigations of hypothalamic regulation of fish thyrotropin (TSH) secretion and subsequent thyroid activity have been impeded by the lack of a reliable assay for TSH. Using a recently developed radioimmunoassay (RIA) for coho salmon TSH we employed an in vitro pituitary cell culture technique to examine regulation of TSH secretion by corticotropin-releasing hormone (CRH) family peptides [ovine CRH (oCRH), carp urotensin I (UI), and frog sauvagine (SV)] as well as thyrotropin-releasing hormone (TRH), salmon growth hormone-releasing hormone (sGHRH), and salmon gonadotropin-releasing hormone (sGnRH). At concentrations of 0.01 to 100 nM, TRH, sGHRH, and sGnRH did not stimulate TSH secretion from coho salmon pituitary cells. However, at these same concentrations, both oCRH and SV caused a significant and concentration-dependent increase in TSH secretion; whereas, UI was highly stimulatory at all concentrations tested. In a related experiment we examined the effect of alpha-helical CRF(9-41) on oCRH-stimulated TSH release by pituitary cells. alpha-Helical CRF(9-41) is an analogue of CRH that has been shown by others to antagonize the adrenocorticotropic hormone (ACTH)-releasing activity of CRH in goldfish. Preincubation of cells with 1 microM alpha-helical CRF(9-41) for 4 h caused a significant suppression of the TSH-releasing activity of oCRH at 1.0 and 10 nM concentrations. The results of these experiments demonstrate the potency of a CRH-like peptide in the hypothalamic regulation of TSH in fish and reveal similarities in the inhibition of the response of both the thyroid and interrenal axis of fish to alpha-helical CRF(9-41).Entities:
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Year: 1998 PMID: 9473372 DOI: 10.1006/gcen.1997.7031
Source DB: PubMed Journal: Gen Comp Endocrinol ISSN: 0016-6480 Impact factor: 2.822