Immunohistochemical localization of BDNF-, TrkB- and TrkA-like proteins in the teleost lateral line system

The lateral line system, formed of both superficial (pit organs) and canal neuromasts, is one of the major mechanosensory systems in fish. It has always been assumed that this system depends on neurotrophins and their cognate Trk receptors for development and maintenance, as has been shown in other...

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Bibliographic Details
Published in:Journal of Anatomy
Main Authors: Germana, A, Catania, S, Cavallaro, M, González-Martínez, T, Ciriaco, E, Hannestad, J, Vega, JA
Format: Text
Language:English
Published: Blackwell Science Inc 2002
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Online Access:http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1570709
http://www.ncbi.nlm.nih.gov/pubmed/12090394
https://doi.org/10.1046/j.1469-7580.2002.00055.x
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Summary:The lateral line system, formed of both superficial (pit organs) and canal neuromasts, is one of the major mechanosensory systems in fish. It has always been assumed that this system depends on neurotrophins and their cognate Trk receptors for development and maintenance, as has been shown in other mechanosensitive systems of vertebrates. However, until now this issue has not been specifically addressed. In this study we used immunohistochemistry to investigate the occurrence and localization both of neurotrophins (NGF-, BDNF- and NT-3-like) and of Trk-like proteins (TrkA-, TrkB-, TrkC-like) in alevins of Salmo salar and S. trutta. All cells in the pit organs of S. salar displayed strong immunoreactivity for TrkB-like and BDNF-like, whereas they were restricted to the hair cells in S. trutta. The hair, supporting and mantle cells of S. salar, and the mantle cells of S. trutta, also expressed TrkA-like immunoreactivity. In the canal neuromasts BDNF-, TrkA- and TrkB-like proteins were present in all cells, without differences between species. NGF-, NT-3- and TrkC-like immunoreactivity were never detected. The present results suggest that mechanoreceptive hair cells, as well as supporting cells, in the lateral line system are under the control of the BDNF–TrkB-like complex, and probably of ligands of TrkA-like receptors.