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Open Access Research article

PLCγ-activated signalling is essential for TrkB mediated sensory neuron structural plasticity

Carla Sciarretta15, Bernd Fritzsch34, Kirk Beisel3, Sonia M Rocha-Sanchez3, Annalisa Buniello1, Jacqueline M Horn2 and Liliana Minichiello12*

Author Affiliations

1 European Molecular Biology Laboratory, Mouse Biology Unit, Via Ramornie 32, 00015 Monterotondo, Rome, Italy

2 Centre for Neuroregeneration, University of Edinburgh, EH16 4SB Edinburgh, UK

3 Creighton University, Department of Biomedical Sciences, Omaha, NE, 68718, USA

4 University of Iowa, Department of Biology, Iowa City, IA, 52242 -1324, USA

5 Actelion Pharmaceuticals, Ltd., Gewerbestrasse 16, CH-4123 Allschwil, Switzerland

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BMC Developmental Biology 2010, 10:103  doi:10.1186/1471-213X-10-103

Published: 8 October 2010



The vestibular system provides the primary input of our sense of balance and spatial orientation. Dysfunction of the vestibular system can severely affect a person's quality of life. Therefore, understanding the molecular basis of vestibular neuron survival, maintenance, and innervation of the target sensory epithelia is fundamental.


Here we report that a point mutation at the phospholipase Cγ (PLCγ) docking site in the mouse neurotrophin tyrosine kinase receptor TrkB (Ntrk2) specifically impairs fiber guidance inside the vestibular sensory epithelia, but has limited effects on the survival of vestibular sensory neurons and growth of afferent processes toward the sensory epithelia. We also show that expression of the TRPC3 cation calcium channel, whose activity is known to be required for nerve-growth cone guidance induced by brain-derived neurotrophic factor (BDNF), is altered in these animals. In addition, we find that absence of the PLCγ mediated TrkB signalling interferes with the transformation of bouton type afferent terminals of vestibular dendrites into calyces (the largest synaptic contact of dendrites known in the mammalian nervous system) on type I vestibular hair cells; the latter are normally distributed in these mutants as revealed by an unaltered expression pattern of the potassium channel KCNQ4 in these cells.


These results demonstrate a crucial involvement of the TrkB/PLCγ-mediated intracellular signalling in structural aspects of sensory neuron plasticity.