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Front Neuroendocrinol. 2015 Jan;36:165-77. doi: 10.1016/j.yfrne.2014.09.004. Epub 2014 Oct 13.

GnRH, anosmia and hypogonadotropic hypogonadism--where are we?

Author information

1
Department of Biological Sciences and the Center for Neuroscience Research, University at Albany, State University of New York, Albany, NY 12222, United States. Electronic address: pforni@albany.edu.
2
Cellular and Developmental Neurobiology Section, National Institute of Neurological Disorders and Stroke, National Institutes of Health, Bethesda, MD 20892, United States. Electronic address: wrays@ninds.nih.gov.

Abstract

Gonadotropin releasing hormone (GnRH) neurons originate the nasal placode and migrate into the brain during prenatal development. Once within the brain, these cells become integral components of the hypothalamic-pituitary-gonadal axis, essential for reproductive function. Disruption of this system causes hypogonadotropic hypogonadism (HH). HH associated with anosmia is clinically defined as Kallman syndrome (KS). Recent work examining the developing nasal region has shed new light on cellular composition, cell interactions and molecular cues responsible for the development of this system in different species. This review discusses some developmental aspects, animal models and current advancements in our understanding of pathologies affecting GnRH. In addition we discuss how development of neural crest derivatives such as the glia of the olfactory system and craniofacial structures control GnRH development and reproductive function.

KEYWORDS:

Craniofacial defects; GnRH; Hypogonadotropic hypogonadism; Hypothalamic–pituitary–gonadal (HPG) axis; Kallmann syndrome; Neural crest; Olfactory ensheathing cells; Olfactory placode; Waardenburg syndrome

PMID:
25306902
PMCID:
PMC4703044
DOI:
10.1016/j.yfrne.2014.09.004
[Indexed for MEDLINE]
Free PMC Article

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