Journal article
PLCγ-activated signalling is essential for TrkB mediated sensory neuron structural plasticity
BMC developmental biology, Vol.10(1), pp.103-103
2010
DOI: 10.1186/1471-213X-10-103
PMID: 20932311
Abstract
Background
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.
Results
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.
Conclusions
These results demonstrate a crucial involvement of the TrkB/PLCγ-mediated intracellular signalling in structural aspects of sensory neuron plasticity.
Details
- Title: Subtitle
- PLCγ-activated signalling is essential for TrkB mediated sensory neuron structural plasticity
- Creators
- Carla Sciarretta - European Molecular Biology Laboratory, Mouse Biology Unit, Via Ramornie 32, 00015 Monterotondo, Rome, ItalyBernd Fritzsch - Creighton University, Department of Biomedical Sciences, Omaha, NE, 68718, USAKirk Beisel - Creighton University, Department of Biomedical Sciences, Omaha, NE, 68718, USASonia M Rocha-Sanchez - Creighton University, Department of Biomedical Sciences, Omaha, NE, 68718, USAAnnalisa Buniello - European Molecular Biology Laboratory, Mouse Biology Unit, Via Ramornie 32, 00015 Monterotondo, Rome, ItalyJacqueline M Horn - Centre for Neuroregeneration, University of Edinburgh, EH16 4SB Edinburgh, UKLiliana Minichiello - European Molecular Biology Laboratory, Mouse Biology Unit, Via Ramornie 32, 00015 Monterotondo, Rome, Italy
- Resource Type
- Journal article
- Publication Details
- BMC developmental biology, Vol.10(1), pp.103-103
- DOI
- 10.1186/1471-213X-10-103
- PMID
- 20932311
- NLM abbreviation
- BMC Dev Biol
- ISSN
- 1471-213X
- eISSN
- 1471-213X
- Publisher
- BioMed Central
- Language
- English
- Date published
- 2010
- Academic Unit
- Iowa Neuroscience Institute; Biology; Craniofacial Anomalies Research Center
- Record Identifier
- 9984070819802771
Metrics
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