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The Journal of Neuroscience, July 22, 2009, 29(29):9390-9395; doi:10.1523/JNEUROSCI.0763-09.2009

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Behavioral/Systems/Cognitive
Regulation of Kiss1 and Dynorphin Gene Expression in the Murine Brain by Classical and Nonclassical Estrogen Receptor Pathways

Michelle L. Gottsch,¹ Víctor M. Navarro,² Zhen Zhao,³ Christine Glidewell-Kenney,⁴ Jeffrey Weiss,⁴ J. Larry Jameson,⁴ Donald K Clifton,¹ Jon E. Levine,³ and Robert A. Steiner^1,2

Departments of ¹Obstetrics and Gynecology and ²Physiology and Biophysics, University of Washington, Seattle, Washington 98195, ³Department of Neurobiology and Physiology, Northwestern University, Evanston, Illinois 60208, and ⁴Division of Endocrinology, Metabolism, and Molecular Medicine, The Feinberg School of Medicine, Northwestern University, Chicago, Illinois 60611

Correspondence should be addressed to Robert A. Steiner, Department of Physiology and Biophysics, University of Washington, Box 357290, Seattle, WA 98195-7290. Email: steiner{at}u.washington.edu

Kisspeptin is a product of the Kiss1 gene and is expressed in the forebrain. Neurons that express Kiss1 play a crucial role in the regulation of pituitary luteinizing hormone secretion and reproduction. These neurons are the direct targets for the action of estradiol-17β (E₂), which acts via the estrogen receptor isoform (ER) to regulate Kiss1 expression. In the arcuate nucleus (Arc), where the dynorphin gene (Dyn) is expressed in Kiss1 neurons, E₂ inhibits the expression of Kiss1 mRNA. However, E₂ induces the expression of Kiss1 in the anteroventral periventricular nucleus (AVPV). The mechanism for differential regulation of Kiss1 in the Arc and AVPV by E₂ is unknown. ER signals through multiple pathways, which can be categorized as either classical, involving the estrogen response element (ERE), or nonclassical, involving ERE-independent mechanisms. To elucidate the molecular basis for the action of E₂ on Kiss1 and Dyn expression, we studied the effects of E₂ on Kiss1 and Dyn mRNAs in the brains of mice bearing targeted alterations in the ER signaling pathways. We found that stimulation of Kiss1 expression by E₂ in the AVPV and inhibition of Dyn in the Arc required an ERE-dependent pathway, whereas the inhibition of Kiss1 expression by E₂ in the Arc involved ERE-independent mechanisms. Thus, distinct ER signaling pathways can differentially regulate the expression of identical genes across different brain regions, and E₂ can act within the same neuron through divergent ER signaling pathways to regulate different neurotransmitter genes.

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Received Feb. 13, 2009; revised June 19, 2009; accepted June 23, 2009.

Correspondence should be addressed to Robert A. Steiner, Department of Physiology and Biophysics, University of Washington, Box 357290, Seattle, WA 98195-7290. Email: steiner{at}u.washington.edu

This article has been cited by other articles:

				J. T. Smith, Q. Li, A. Pereira, and I. J. Clarke Kisspeptin Neurons in the Ovine Arcuate Nucleus and Preoptic Area Are Involved in the Preovulatory Luteinizing Hormone Surge Endocrinology, December 1, 2009; 150(12): 5530 - 5538. [Abstract] [Full Text] [PDF]

				A. E. Oakley, D. K. Clifton, and R. A. Steiner Kisspeptin Signaling in the Brain Endocr. Rev., October 1, 2009; 30(6): 713 - 743. [Abstract] [Full Text] [PDF]

				V. M. Navarro, M. L. Gottsch, C. Chavkin, H. Okamura, D. K. Clifton, and R. A. Steiner Regulation of Gonadotropin-Releasing Hormone Secretion by Kisspeptin/Dynorphin/Neurokinin B Neurons in the Arcuate Nucleus of the Mouse J. Neurosci., September 23, 2009; 29(38): 11859 - 11866. [Abstract] [Full Text] [PDF]

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