Article

Regulation of the neuroendocrine reproductive axis by kisspeptin-GPR54 signaling.

Physiology and Biophysics and Obstetrics and Gynecology, University of Washington, Seattle, Washington 98195-7290, USA.
Reproduction (Cambridge, England) (impact factor: 3.09). 05/2006; 131(4):623-30. DOI:10.1530/rep.1.00368 pp.623-30
Source: PubMed

ABSTRACT The Kiss1 gene codes for a family of peptides that act as endogenous ligands for the G protein-coupled receptor GPR54. Spontaneous mutations or targeted deletions of GPR54 in man and mice produce hypogonadotropic hypogonadism and infertility. Centrally administered kisspeptins stimulate gonadotropin secretion by acting directly on GnRH neurons. Sex steroids regulate the expression of KiSS-1 mRNA in the brain through direct action on KiSS-1 neurons. In the arcuate nucleus (Arc), sex steroids inhibit the expression of KiSS-1, suggesting that these neurons serve as a conduit for the negative feedback regulation of gonadotropin secretion. In the anteroventral periventricular nucleus (AVPV), sex steroids induce the expression of KiSS-1, implying that KiSS-1 neurons in this region may have a role in the preovulatory LH surge (in the female) or sexual behavior (in the male).

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Keywords

anteroventral periventricular nucleus
 
arcuate nucleus
 
conduit
 
deletions
 
direct action
 
endogenous ligands
 
G protein-coupled receptor GPR54
 
GnRH neurons
 
gonadotropin secretion
 
hypogonadotropic hypogonadism
 
KiSS-1 neurons
 
Kiss1 gene codes
 
kisspeptins stimulate gonadotropin secretion
 
negative feedback regulation
 
neurons
 
peptides
 
preovulatory LH surge
 
Sex steroids
 
sexual behavior
 

Jeremy T Smith