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This version published online on June 20, 2003
Molecular Endocrinology, doi:10.1210/me.2003-0040
Molecular Endocrinology Vol. 0, No. 2003 200300401-
doi:10.1210/me.2003-0040
Copyright © 2003 by the Endocrine Society.
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Submitted on February 5, 2003
Accepted on June 12, 2003

Regulation of Cyclic AMP Signaling and Pulsatile Neurosecretion by Gi-coupled Plasma Membrane Estrogen Receptors in Immortalized GnRH Neurons

Carlos E. Navarro1, Sheikh Abdul Saeed1, Cynthia Murdock1, Antonio J. Martinez-Fuentes1, Krishan K. Arora1, Lazar Z. Krsmanovic1, and Kevin J. Catt1*

1 Endocrinology and Reproduction Research Branch, National Institute of Child Health and Human Development, NIH, Bethesda, MD 20892-4510

* To whom correspondence should be addressed. E-mail: catt{at}helix.nih.gov.

Immortalized GnRH neurons (GT1-7) express receptors for estrogen (ER{alpha} and ER{beta}) and progesterone (PRA), and exhibit positive immunostaining for both intracellular and plasma membrane ERs. Exposure of GT1-7 cells to picomolar estradiol concentrations for 5-60 min caused rapid, sustained, and dose-dependent inhibition of cAMP production. In contrast, treatment with nanomolar estradiol concentrations for 60 min increased cAMP production. The inhibitory and stimulatory actions of estradiol on cAMP formation were abolished by the ER antagonist, ICI 182,780. The estradiol-induced inhibition of cAMP production was prevented by treatment with pertussis toxin, consistent with coupling of the plasma membrane ER to an inhibitory G protein. Coimmunoprecipitation studies demonstrated an E2-regulated stimulatory interaction between ER{alpha} and G{alpha}i3 that was prevented by the ER antagonist, ICI 182,780. Exposure of perifused GT1-7 cells and hypothalamic neurons to picomolar estradiol levels increased the GnRH peak interval, shortened peak duration, and increased peak amplitude. These findings indicate that occupancy of the plasma membrane-associated ERs expressed in GT1-7 neurons by physiological estradiol levels causes activation of a Gi protein and modulates cAMP signaling and neuropeptide secretion.

NURSA Molecule Pages Link:

Nuclear Receptors:   ERα  |  ERβ  |  PR
Ligands:   17β-Estradiol  |  Progesterone



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