Document Detail


Oestrogen induces rhythmic expression of the Kisspeptin-1 receptor GPR54 in hypothalamic gonadotrophin-releasing hormone-secreting GT1-7 cells.
MedLine Citation:
PMID:  21756268     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
Oestrogen-stimulated preovulatory gonadotrophin surges are temporally regulated in a way that remains not fully understood. Mammalian ovulation requires surges of gonadotrophin-releasing hormone (GnRH), released from specialised neurones in the hypothalamus. Surge regulation is mediated by ovarian oestrogen (17 β-oestradiol; E(2) ) feedback-acting as a negative signal until the early afternoon of the pro-oestrous phase, at which point it stimulates robust increases in GnRH release. Multiple lines of evidence suggest a role for the circadian clock in surge generation, although the presence of endogenous oscillators in several neuronal populations throughout the mediobasal hypothalamus complicates an elucidation of the underlying mechanisms of circadian regulation. In the present study, we propose that endogenous oscillators within GnRH neurones are modulated by oestrogen to elicit GnRH surge secretion. One mechanism by which this may occur is through the up-regulation of receptors of known stimulators of GnRH, such as kisspeptin's cognate receptor, GPR54. Through analysis of mRNA and protein abundance patterns, we found that high levels of E(2) elicit circadian expression profiles of GPR54 in vitro, and that disruption of endogenous GnRH oscillators of the clock dampens this effect. Additionally, although kisspeptin administration to GT1-7 cells does not result in surge-level secretion, we observed increased GnRH secretion from GT1-7 cells treated with positive feedback levels of E(2) . These results in this in vitro neuronal model system suggest a possible mechanism whereby receptor expression levels, and thus GnRH sensitivity to kisspeptin, may change dramatically over the pro-oestrous day. In this way, elevated ovarian E(2) may increase kisspeptidergic tone at the same time as increasing GnRH neuronal sensitivity to this neuropeptide for maximal surge release.
Authors:
K J Tonsfeldt; C P Goodall; K L Latham; P E Chappell
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Publication Detail:
Type:  Journal Article; Research Support, N.I.H., Extramural    
Journal Detail:
Title:  Journal of neuroendocrinology     Volume:  23     ISSN:  1365-2826     ISO Abbreviation:  J. Neuroendocrinol.     Publication Date:  2011 Sep 
Date Detail:
Created Date:  2011-08-12     Completed Date:  2012-02-17     Revised Date:  2013-06-28    
Medline Journal Info:
Nlm Unique ID:  8913461     Medline TA:  J Neuroendocrinol     Country:  England    
Other Details:
Languages:  eng     Pagination:  823-30     Citation Subset:  IM    
Copyright Information:
© 2011 The Authors. Journal of Neuroendocrinology © 2011 Blackwell Publishing Ltd.
Affiliation:
Department of Biomedical Sciences, College of Veterinary Medicine, Oregon State University, Corvallis, OR 97331, USA.
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MeSH Terms
Descriptor/Qualifier:
Animals
Cell Line / drug effects*
Circadian Rhythm / drug effects*
Estradiol / pharmacology*
Female
Gonadotropin-Releasing Hormone / secretion*
Kisspeptins / metabolism
Mice
Receptors, G-Protein-Coupled / genetics,  metabolism*
Grant Support
ID/Acronym/Agency:
R01 DK073571-05/DK/NIDDK NIH HHS; R01 HD065331-06A1/HD/NICHD NIH HHS; R01DK073571/DK/NIDDK NIH HHS
Chemical
Reg. No./Substance:
0/Kiss1r protein, mouse; 0/Kisspeptins; 0/Receptors, G-Protein-Coupled; 33515-09-2/Gonadotropin-Releasing Hormone; 50-28-2/Estradiol
Comments/Corrections

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