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Immortalized Luteinizing Hormone-Releasing Hormone Neurons Show a Different Migratory Activity in Vitro¹

Department of Endocrinology (R.M., F.P., L.Mo., L.Ma., F.P.), University of Milano, Milano 20133, Italy; and Department of Surgical Pathology and Cytopathology (M.M.), "A. Manzoni" Hospital Lecco 23900, LC, Italy

Address all correspondence and requests for reprints to: Roberto Maggi, Ph.D., Istituto di Endocrinologia, Università degli Studi di Milano, Via G. Balzaretti, 9, 20133 Milano, Italy. E-mail: Roberto.Maggi{at}unimi.it

The development of two cell lines (GT1 and GN) of immortalized LHRH neurons has allowed an accurate study of the mechanisms controlling the synthesis and the secretion of LHRH. These cell lines, obtained in mice by genetic targeted tumorigenesis, retain many of the phenotypic characteristics of LHRH neurons. Of interest, GT1 cells derive from an hypothalamic tumor, whereas GN cells were obtained from a tumor localized in the olfactory bulb. The different origin of these cell lines lead to hypothesize that they might represent hypothalamic postmigratory neurons (GT1 cells), or LHRH neurons blocked at an early stage of their migration (GN cells). Using different experimental procedures, we found that the two cell subclones GT1–7 and GN11 express a different morphology and migratory behavior in vitro. In particular, we found that GN11 cells, but not GT1–7 cells, show the morphological shape of migrating neurons. When analyzing the spontaneous motility we found that only GN11 cells express a high capacity of migrating in a matrix of collagen gel. Moreover, in a chemomigratory assay GN11 cells did show a significant response to the chemotactic stimulus represented by the FBS. On the contrary, GT1–7 cells show very low spontaneous motility and appear insensitive to the FBS stimulus. These results suggest that the simultaneous use of the GT1–7/GN11 cells may represent an experimental tool for screening the factors possibly involved in the control of the migratory processes of LHRH neurons in normal and in pathological conditions, such as those due to their impaired migration, like it happens in Kallmann’s syndrome.

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