title: Glial-gonadotrophin hormone (GnRH) neurone interactions in the median eminence and the control of GnRH secretion.
abstract: A wealth of information now exists showing that glial cells are actively involved in the cell-cell communication process generating and disseminating information within the central nervous system. In the hypothalamus, two types of glial cells, astrocytes and ependymal cells lining the latero-ventral portion of the third ventricle (known as tanycytes), regulate the secretory activity of neuroendocrine neurones. This function, initially described for astrocytes apposing magnocellular neurones, has been more recently characterised for neurones secreting gonadotrophin hormone-releasing hormone (GnRH). The available evidence suggests that glial cells of the median eminence regulate GnRH secretion via two related mechanisms. One involves the production of growth factors acting via receptors with tyrosine kinase activity. The other involves plastic rearrangements of glia-GnRH neurone adhesiveness. GnRH axons reach the median eminence, at least in part, directed by basic fibroblast growth factor. Their secretory activity is facilitated by insulin-like growth factor 1 and members of the epidermal growth factor family. A structural complement to these soluble molecules is provided by at least three cell-cell adhesion systems endowed with signalling capabilities. One of them uses the neuronal cell adhesion molecule (NCAM), another employs the synaptic cell adhesion molecule (SynCAM), and the third one consists of neuronal contactin interacting with glial receptor-like protein tyrosine phosphatase-beta. It is envisioned that, within the median eminence, soluble factors and adhesion molecules work coordinately to control delivery of GnRH to the portal vasculature.
authors.affiliation: Division of Neuroscience, Oregon National Primate Research Center, Oregon Health and Science University, Beaverton, OR 97006, USA.
authors.forename: S R
authors.initials: SR
authors.lastname: Ojeda
authors.forename: A
authors.initials: A
authors.lastname: Lomniczi
authors.forename: U S
authors.initials: US
authors.lastname: Sandau
mesh_terms: D000818:Animals; D015816:Cell Adhesion Molecules, Neuronal / Q000378:metabolism; D002450:Cell Communication / Q000502:physiology*; D048430:Cell Shape; D004815:Epidermal Growth Factor / Q000378:metabolism; D018698:Glutamic Acid / Q000378:metabolism; D007987:Gonadotropin-Releasing Hormone / Q000378:metabolism*; D007334:Insulin-Like Growth Factor I / Q000378:metabolism; D008473:Median Eminence / Q000166:cytology / Q000378:metabolism*; D009457:Neuroglia / Q000166:cytology / Q000378:metabolism*; D009473:Neuronal Plasticity / Q000502:physiology; D009474:Neurons / Q000166:cytology / Q000378:metabolism*; D054633:Receptor-Like Protein Tyrosine Phosphatases, Class 5 / Q000378:metabolism
chemical_list: D015816:Cell Adhesion Molecules, Neuronal; D007987:Gonadotropin-Releasing Hormone; D018698:Glutamic Acid; D004815:Epidermal Growth Factor; D007334:Insulin-Like Growth Factor I; D054633:Receptor-Like Protein Tyrosine Phosphatases, Class 5