This Article Full Text Full Text (PDF) Purchase Article View Shopping Cart Alert me when this article is cited Alert me if a correction is posted Citation Map Services Email this article to a friend Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Request Copyright Permission Citing Articles Citing Articles via HighWire Citing Articles via Google Scholar Google Scholar Articles by Li, X. F. Articles by O’Byrne, K. T. Search for Related Content PubMed PubMed Citation Articles by Li, X. F. Articles by O’Byrne, K. T.

Role of Corticotropin-Releasing Factor Receptor-2 in Stress-Induced Suppression of Pulsatile Luteinizing Hormone Secretion in the Rat

Division of Reproductive Health, Endocrinology, and Development (X.F.L., J.E.B., K.T.O.), New Hunt’s House, King’s College London, London SE1 1UL, United Kingdom; and Henry Wellcome Laboratory for Integrative Neuroscience and Endocrinology (S.L.L.), University of Bristol, Bristol BS1 3NY, United Kingdom

Address all correspondence and requests for reprints to: Dr. Kevin O’Byrne, Division of Reproductive Health, Endocrinology, and Development, 2.36D New Hunt’s House, King’s College London, Guy’s Campus, London SE1 1UL, United Kingdom. E-mail: kevin.o'byrne{at}kcl.ac.uk.

Corticotropin-releasing factor (CRF) has been implicated as an important mediator of stress-induced inhibition of reproduction. The role of specific CRF receptor subtypes in this effect is unknown, and in the current study, we investigated the role of the CRF-R2 receptor in stress-mediated suppression of pulsatile LH section. Ovariectomized rats with sc 17ß-estradiol capsules were implanted with intracerebroventricular (icv) and iv cannulae. Blood samples (25 µl) were collected every 5 min for 5 h for LH measurement. Central administration of urocortin II (0.24, 2.4, 24, or 240 nmol, icv), which selectively binds to CRF-R2, resulted in a dose-dependent suppression of LH pulses. Restraint stress (1 h) induced a profound suppression of pulsatile LH secretion and astressin₂-B, a selective CRF-R2 antagonist (28 nmol icv, 10-min prerestraint), was effective in blocking this inhibitory response. These findings suggest that CRF-R2 mediates, at least in part, restraint stress-induced inhibition of LH pulses and may play a pivotal role in the normal physiological response of stress-induced suppression of the hypothalamic GnRH pulse generator and hence the reproductive system.

This article has been cited by other articles:

				C. L. Rivier Urocortin 1 Inhibits Rat Leydig Cell Function Endocrinology, December 1, 2008; 149(12): 6425 - 6432. [Abstract] [Full Text] [PDF]

				X. F. Li, J. S. Kinsey-Jones, A. M. I. Knox, X. Q. Wu, D. Tahsinsoy, S. D. Brain, S. L. Lightman, and K. T. O'Byrne Neonatal Lipopolysaccharide Exposure Exacerbates Stress-Induced Suppression of Luteinizing Hormone Pulse Frequency in Adulthood Endocrinology, December 1, 2007; 148(12): 5984 - 5990. [Abstract] [Full Text] [PDF]

				T. Matsuwaki, Y. Kayasuga, K. Yamanouchi, and M. Nishihara Maintenance of Gonadotropin Secretion by Glucocorticoids under Stress Conditions through the Inhibition of Prostaglandin Synthesis in the Brain Endocrinology, March 1, 2006; 147(3): 1087 - 1093. [Abstract] [Full Text] [PDF]