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Neuroendocrinology. 2014;100(1):71-80. doi: 10.1159/000365574. Epub 2014 Jul 7.

Activation of the GPR30 receptor promotes lordosis in female mice.

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1
Neuroscience Program, Tulane University, New Orleans, La., USA.

Abstract

BACKGROUND/AIMS:

Estrogens are important effectors of reproduction and are critical for upregulating female reproductive behavior or lordosis in females. In addition to the importance of transcriptional regulation of genes by 17β-estradiol-bound estrogen receptors (ER), extranuclear signal transduction cascades such as protein kinase A (PKA) are also important in regulating female sexual receptivity. GPR30 (G-protein coupled receptor 30), also known as GPER1, a putative membrane ER (mER), is a G protein-coupled receptor that binds 17β-estradiol with an affinity that is similar to that possessed by the classical nuclear ER and activates both PKA and extracellular-regulated kinase signaling pathways. The high expression of GPR30 in the ventromedial hypothalamus, a region important for lordosis behavior as well as kinase cascades activated by this receptor, led us to hypothesize that GPR30 may regulate lordosis behavior in female rodents.

METHOD:

In this study, we investigated the ability of G-1, a selective agonist of GPR30, to regulate lordosis in the female mouse by administering this agent prior to progesterone in an estradiol-progesterone priming paradigm prior to testing with stud males.

RESULTS:

As expected, 17β-estradiol benzoate (EB), but not sesame oil, increased lordosis behavior in female mice. G-1 also increased lordosis behavior in female mice and decreased the number of rejective responses towards male mice, similar to the effect of EB. The selective GPR30 antagonist G-15 blocked these effects.

CONCLUSION:

This study demonstrates that activation of the mER GPR30 stimulates social behavior in a rodent model in a manner similar to EB.

PMID:
25012534
DOI:
10.1159/000365574
[Indexed for MEDLINE]

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