In vivo and in vitro localization of brain-derived neurotrophic factor, fibroblast growth factor-2 and their receptors in the bullfrog vestibular end organs.

Brain Res Mol Brain Res

Victor Goodhill Ear Center, Division of Head and Neck Surgery, University of California, Los Angeles School of Medicine, CHS, Room 62-129, 10833 Le Conte Ave., Los Angeles, CA 90095-1624, USA.

Published: June 2002

The inner ear sensory epithelia of vertebrates are composed mainly of supporting cells and hair cells (HCs). Brain-derived neurotrophic factor (BDNF) and fibroblast growth factor-2 (FGF-2) are trophins that are believed to play an essential role in the development and innervation of inner ear epithelia. Both trophins also may play a crucial role in the maintenance and regeneration of hair cells in the adult vertebrate ear. In the bullfrog vestibular system, hair cells are produced throughout life, and the epithelia regenerates following ototoxicity. The expression of BDNF and FGF-2 in the vestibular organs of the adult bullfrog was investigated at a cellular level both in histological sections and in vitro in dissociated cell cultures. In histological sections of the crista ampullaris, in situ hybridization and immunocytochemical techniques demonstrated that HCs express both BDNF and its receptor trkB, while the supporting cells express the receptor trkB alone. Following dissociation and in vitro cell culture no changes in the pattern of BDNF and trkB receptor were observed. Immunocytochemical studies demonstrated that in vivo hair cells express FGF-2 and the receptors FGFR-1 and FGFR-2 while supporting cells do not express either molecule. Following dissociation, HCs continue to express FGF-2 and its two receptors, while supporting cells upregulate the expression of FGF-2 and its receptor FGFR-2. These data confirm the potential role of BDNF and FGF-2 trophic regulation of the sensory epithelia of the adult inner ear. The findings suggest that BDNF has a role in the maintenance of the vestibular epithelia while FGF-2 may regulate the proliferation of supporting cells.

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http://dx.doi.org/10.1016/s0169-328x(02)00202-4DOI Listing

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