title: Activation of the GPR30 receptor promotes lordosis in female mice.
abstract: OBJECTIVE
  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.
  
  
  METHODS
  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.
  
  
  CONCLUSIONS
  This study demonstrates that activation of the mER GPR30 stimulates social behavior in a rodent model in a manner similar to EB.
authors.affiliation: Neuroscience Program, Tulane University, New Orleans, La., USA.
authors.forename: Divya
authors.initials: D
authors.lastname: Anchan
authors.forename: Amber
authors.initials: A
authors.lastname: Gafur
authors.forename: Kazuhiro
authors.initials: K
authors.lastname: Sano
authors.forename: Sonoko
authors.initials: S
authors.lastname: Ogawa
authors.forename: Nandini
authors.initials: N
authors.lastname: Vasudevan
mesh_terms: D000818:Animals; D003517:Cyclopentanes / Q000494:pharmacology; D004958:Estradiol / Q000031:analogs & derivatives / Q000494:pharmacology; D004967:Estrogens / Q000494:pharmacology; D005260:Female; D008810:Mice, Inbred C57BL; D011187:Posture / Q000502:physiology*; D011374:Progesterone / Q000494:pharmacology; D011372:Progestins / Q000494:pharmacology; D011804:Quinolines / Q000494:pharmacology; D011897:Random Allocation; D011960:Receptors, Estrogen; D043562:Receptors, G-Protein-Coupled / Q000819:agonists / Q000378:metabolism*; D012102:Reproductive Control Agents / Q000494:pharmacology; D012726:Sexual Behavior, Animal / Q000187:drug effects / Q000502:physiology*
chemical_list: C517943:1-(4-(6-bromobenzo(1,3)dioxol-5-yl)-3a,4,5,9b-tetrahydro-3H-cyclopenta(c)quinolin-8-yl)ethanone; D003517:Cyclopentanes; D004967:Estrogens; C532507:GPER1 protein, mouse; D011372:Progestins; D011804:Quinolines; D011960:Receptors, Estrogen; D043562:Receptors, G-Protein-Coupled; D012102:Reproductive Control Agents; C074283:estradiol 3-benzoate; D011374:Progesterone; D004958:Estradiol