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Focal delivery of fibroblast growth factor‐1 by transfected cells induces spiral ganglion neurite targeting in vitro
Author(s) -
Dazert S.,
Kim D.,
Luo L.,
Aletsee C.,
Garfunkel S.,
Maciag T.,
Baird A.,
Ryan A. F.
Publication year - 1998
Publication title -
journal of cellular physiology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.529
H-Index - 174
eISSN - 1097-4652
pISSN - 0021-9541
DOI - 10.1002/(sici)1097-4652(199810)177:1<123::aid-jcp13>3.0.co;2-e
Subject(s) - neurite , transfection , in vitro , microbiology and biotechnology , spiral ganglion , fibroblast , nerve growth factor , fibroblast growth factor , chemistry , spiral (railway) , anatomy , biology , cell culture , receptor , biochemistry , genetics , inner ear , mathematical analysis , mathematics
Sensory cells in the cochlea of the rat transiently express acidic fibroblast growth factor (FGF‐1) during the developmental period of terminal innervation in the sensory epithelium. To explore the potential role of FGF‐1 in terminal innervation events, the response of cochlear ganglion neurons to FGF‐1 was evaluated in culture. Explants from the spiral ganglion of postnatal day 5 rats were cultured in the presence of exogenous FGF‐1, with or without heparin. FGF‐1 in the culture medium produced a dose‐dependent increase in the number and length of neurites produced by spiral ganglion neurons, a response that was enhanced by heparin. To assess the effects of FGF‐1 produced by a focal, cellular source, additional explants were cocultured with 3T3 cell transfectants that secrete FGF‐1. Neurites that came into contact with FGF‐1 secreting cells branched, formed bouton‐like terminal swellings on the surface of the transfectants, and stopped extending. The results suggest that FGF‐1 may stimulate neurite extension into the sensory epithelium of the cochlea and that focal production of FGF‐1 may contribute to the formation of contacts on sensory cells by developing neurites. J. Cell. Physiol. 177:123–129, 1998. © 1998 Wiley‐Liss, Inc.