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First published online 26 October 2004
doi: 10.1242/jcs.01511

Journal of Cell Science 117, 5803-5814 (2004)
Published by The Company of Biologists 2004
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Research Article

Truncated TrkB receptor-induced outgrowth of dendritic filopodia involves the p75 neurotrophin receptor

Matthias Hartmann1,2, Tanja Brigadski1, Kai S. Erdmann2, Bettina Holtmann3, Michael Sendtner3, Frank Narz2 and Volkmar Leßmann1,*

1 Institute of Physiology and Pathophysiology, Johannes Gutenberg-University Mainz, Duesbergweg 6, 55128 Mainz, Germany
2 Department of Molecular Neurobiochemistry, Ruhr-University Bochum, Universitätsstraße 150, 44801 Bochum, Germany
3 Institute for Clinical Neurobiology, Julius-Maximilians University Würzburg, Sanderring 2 - 97070 Würzburg, Germany

* Author for correspondence (e-mail: lessmann{at}uni-mainz.de)

Accepted 24 August 2004

The Trk family of receptor tyrosine kinases and the p75 receptor (p75NTR) mediate the effects of neurotrophins on neuronal survival, differentiation and synaptic plasticity. The neurotrophin BDNF and its cognate receptor tyrosine kinase, TrkB.FL, are highly expressed in neurons of the central nervous system. At later stages in postnatal development the truncated TrkB splice variants (TrkB.T1, TrkB.T2) become abundant. However, the signalling and function of these truncated receptors remained largely elusive.

We show that overexpression of TrkB.T1 in hippocampal neurons induces the formation of dendritic filopodia, which are known precursors of synaptic spines. The induction of filopodia by TrkB.T1 occurs independently of neurotrophin binding and of kinase activity of endogenous TrkB.FL. Coexpression of a p75NTR lacking an intracellular domain inhibits the TrkB.T1-induced effect in a dominant negative manner. Steric hindrance of extracellular p75NTR interactions with a specific antibody, or absence of p75NTR with an intact extracellular domain also inhibit this TrkB.T1-induced effect.

We thus propose a novel signalling pathway initiated by neurotrophin-independent extracellular or intramembrane interaction of TrkB.T1 with the p75NTR receptor, which modulates dendritic growth via p75NTR signalling cascades.

Key words: Neurotrophins, Trk, p75 receptor, Filopodia, BDNF, Spines




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