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J. Biol. Chem., Vol. 279, Issue 1, 117-126, January 2, 2004

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Expression and Function of Gonadotropin-releasing Hormone (GnRH) Receptor in Human Olfactory GnRH-secreting Neurons

AN AUTOCRINE GnRH LOOP UNDERLIES NEURONAL MIGRATION^*

Roberto Giulio Romanelli, Tullio Barni, Mario Maggi¶, Michaela Luconi¶, Paola Failli||, Anna Pezzatini**, Elisabetta Pelo, Francesca Torricelli, Clara Crescioli, Pietro Ferruzzi, Roberto Salerno, Mirca Marini**, Carlo Maria Rotella, and Gabriella B. Vannelli**¶¶

From the ^**Departments of Anatomy Histology and Forensic Medicine and Clinical Physiopathology and Endocrinology and ^¶Andrology Unit and Genetic Unit, Departments of Internal Medicine and ^||Preclinical and Clinical Pharmacology, University of Florence, School of Medicine, Florence I-50134, Italy and Department of Experimental and Clinical Medicine, University of Catanzaro, Catanzaro I-88100, Italy

Olfactory neurons and gonadotropin-releasing hormone (GnRH) neurons share a common origin during organogenesis. Kallmann's syndrome, clinically characterized by anosmia and hypogonadotropic hypogonadism, is due to an abnormality in the migration of olfactory and GnRH neurons. We recently characterized the human FNC-B4 cell line, which retains properties present in vivo in both olfactory and GnRH neurons. In this study, we found that FNC-B4 neurons expressed GnRH receptor and responded to GnRH with time- and dose-dependent increases in GnRH gene expression and protein release (up to 5-fold). In addition, GnRH and its analogs stimulated cAMP production and calcium mobilization, although at different biological thresholds (nanomolar for cAMP and micromolar concentrations for calcium). We also observed that GnRH triggered axon growth, actin cytoskeleton remodeling, and a dose-dependent increase in migration (up to 3–4-fold), whereas it down-regulated nestin expression. All these effects were blocked by a specific GnRH receptor antagonist, cetrorelix. We suggest that GnRH, secreted by olfactory neuroblasts, acts in an autocrine pattern to promote differentiation and migration of those cells that diverge from the olfactory sensory lineage and are committed to becoming GnRH neurons.

Received for publication, July 22, 2003 , and in revised form, September 18, 2003.

^* This work was supported by grants from the Ministero dell'Istruzione, dell'Università e della Ricerca (MIUR) and from the University of Florence. The costs of publication of this article were defrayed in part by the payment of page charges. This article must therefore be hereby marked "advertisement" in accordance with 18 U.S.C. Section 1734 solely to indicate this fact.

^¶¶ To whom correspondence should be addressed: Dept. of Anatomy Histology and Forensic Medicine, University of Florence, School of Medicine, V.le Morgagni 85, I-50134 Florence, Italy. Tel.: 39-55-410084; Fax: 39-55-4379500; E-mail: vannelli{at}unifi.it.

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