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Publication : PLCĪ³-activated signalling is essential for TrkB mediated sensory neuron structural plasticity.

First Author  Sciarretta C Year  2010
Journal  BMC Dev Biol Volume  10
Pages  103 PubMed ID  20932311
Mgi Jnum  J:166067 Mgi Id  MGI:4839672
Doi  10.1186/1471-213X-10-103 Citation  Sciarretta C, et al. (2010) PLCgamma-activated signalling is essential for TrkB mediated sensory neuron structural plasticity. BMC Dev Biol 10:103
abstractText  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 Cgamma (PLCgamma) 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 PLCgamma 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/PLCgamma-mediated intracellular signalling in structural aspects of sensory neuron plasticity.
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