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This Article Full Text Full Text (PDF) All Versions of this Article: JOE-08-0139v1 200/2/223    most recent Alert me when this article is cited Alert me if a correction is posted Services Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Citing Articles Citing Articles via HighWire Citing Articles via Google Scholar Google Scholar Articles by Seasholtz, A. F Articles by Thompson, R. C Search for Related Content PubMed PubMed Citation Articles by Seasholtz, A. F Articles by Thompson, R. C

¹ Molecular and Behavioral Neuroscience Institute, University of Michigan, 109 Zina Pitcher Place, BSRB Room 5035, Ann Arbor, Michigan 48109, USA
² Department of Biological Chemistry, University of Michigan, 109 Zina Pitcher Place, BSRB Room 5035, Ann Arbor, Michigan 48109, USA
³ Department of Psychiatry, University of Michigan, 109 Zina Pitcher Place, BSRB Room 5035, Ann Arbor, Michigan 48109, USA

(Correspondence should be addressed to A F Seasholtz; Email: aseashol{at}umich.edu)

(M Öhman is now at Department of Internal Medicine, Cardiology, University of Michigan, Ann Arbor, Michigan, USA)

Corticotropin-releasing hormone (CRH) is a key regulator of the mammalian stress response, mediating a wide variety of stress-associated behaviors including stress-induced inhibition of reproductive function. To investigate the potential direct action of CRH on pituitary gonadotrope function, we examined CRH receptor expression and second messenger signaling in T3-1 cells, a murine gonadotrope-like cell line. Reverse transcriptase PCR (RT-PCR) studies demonstrated that T3-1 cells express mRNA for the two CRH receptor subtypes, CRHR1 and CRHR2, with CRHR2 as the predominant CRHR2 isoform. Stimulation of the cells with CRH or urocortin (UCN) resulted in rapid, transient increases in the intracellular levels of cAMP that were completely blocked by the addition of -helical CRH 9-41 or astressin, non-selective CRH receptor antagonists. Stimulation of the cells with CRHR2-specific ligands, urocortin 2 (UCN2) or urocortin 3 (UCN3), resulted in rapid increases in intracellular cAMP levels to 50–60% of the levels observed with UCN. Treatment with a selective CRHR2 antagonist, antisauvagine, completely blocked UCN3-mediated increases in cAMP and significantly reduced, but did not completely block UCN-mediated increases in cAMP, demonstrating that both CRHR1 and CRHR2 are functionally active in these gonadotrope-like cells. Finally, UCN treatment significantly increased the transcriptional activity of the glycoprotein hormone -subunit promoter as assessed by -luciferase transfection assays. Together, these results demonstrate the functional signaling of CRH receptors in T3-1 cells, suggesting that CRH may also modulate pituitary gonadotrope function in vivo.

This article has been cited by other articles:

				R. T. Evans and A. F. Seasholtz Soluble Corticotropin-Releasing Hormone Receptor 2{alpha} Splice Variant Is Efficiently Translated But Not Trafficked for Secretion Endocrinology, September 1, 2009; 150(9): 4191 - 4202. [Abstract] [Full Text] [PDF]