Regulation of the neuroendocrine reproductive axis by kisspeptin-GPR54 signaling

Jeremy Smith, Donald K. Clifton, Robert A. Steiner

Research output: Contribution to journalReview article

180 Citations (Scopus)

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).

Original languageEnglish
Pages (from-to)623-630
Number of pages8
JournalReproduction
Volume131
Issue number4
DOIs
Publication statusPublished - Apr 2006
Externally publishedYes

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