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Involvement of G Protein-Coupled Receptor 30 (GPR30) in Rapid Action of Estrogen in Primate LHRH Neurons

By Sekoni D. Noel, Kim L. Keen, David I. Baumann, Edward J. Filardo and Ei Terasawa

Abstract

Previously, we have reported that 17β-estradiol (E2) induces an increase in firing activity of primate LH-releasing hormone (LHRH) neurons. The present study investigates whether E2 alters LHRH release as well as the pattern of intracellular calcium ([Ca2+]i) oscillations and whether G protein-coupled receptor 30 (GPR30) plays a role in mediating the rapid E2 action in primate LHRH neurons. Results are summarized: 1) E2, the nuclear membrane-impermeable estrogen, estrogen-dendrimer conjugate, and the plasma membrane-impermeable estrogen, E2-BSA conjugate, all stimulated LHRH release within 10 min of exposure; 2) whereas the estrogen receptor antagonist, ICI 182,780, did not block the E2-induced LHRH release, E2 application to cells treated with pertussis toxin failed to induce LHRH release; 3) GPR30 mRNA was expressed in olfactory placode cultures, and GPR30 protein was expressed in a subset of LHRH neurons; 4) pertussis toxin treatment blocked the E2-induced increase in [Ca2+]i oscillations; 5) knockdown of GPR30 in primate LHRH neurons by transfection with small interfering RNA (siRNA) for GPR30 completely abrogated the E2-induced changes in [Ca2+]i oscillations, whereas transfection with control siRNA did not; 6) the estrogen-dendrimer conjugate-induced increase in [Ca2+]i oscillations also did not occur in LHRH neurons transfected with GPR30 siRNA; and 7) G1, a GPR30 agonist, resulted in changes in [Ca2+]i oscillations, similar to those observed with E2. Collectively, E2 induces a rapid excitatory effect on primate LHRH neurons, and this rapid action of E2 appears to be mediated, in part, through GPR30

Topics: Article
Publisher: The Endocrine Society
OAI identifier: oai:pubmedcentral.nih.gov:2654512
Provided by: PubMed Central
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