Neurotrophin receptors TrkA and TrkC cause neuronal death whereas TrkB does not

Vassiliki Nikoletopoulou (), Heiko Lickert, José Maria Frade, Chantal Rencurel, Patrizia Giallonardo, Lixin Zhang, Miriam Bibel and Yves-Alain Barde ()
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Vassiliki Nikoletopoulou: Biozentrum, University of Basel
Heiko Lickert: Helmholtz Zentrum München, Institute of Stem Cell Research, Ingolstädter Landstrasse 1, D-85764 Neuherberg, Germany
José Maria Frade: Instituto Cajal, CSIC
Chantal Rencurel: Biozentrum, University of Basel
Patrizia Giallonardo: Helmholtz Zentrum München, Institute of Stem Cell Research, Ingolstädter Landstrasse 1, D-85764 Neuherberg, Germany
Lixin Zhang: Biozentrum, University of Basel
Miriam Bibel: Neuroscience Research, Novartis Institutes for BioMedical Research
Yves-Alain Barde: Biozentrum, University of Basel

Nature, 2010, vol. 467, issue 7311, 59-63

Abstract: Abstract Neurons of the peripheral nervous system have long been known to require survival factors to prevent their death during development. But why they selectively become dependent on secretory molecules has remained a mystery, as is the observation that in the central nervous system, most neurons do not show this dependency. Using engineered embryonic stem cells, we show here that the neurotrophin receptors TrkA and TrkC (tropomyosin receptor kinase A and C, also known as Ntrk1 and Ntrk3, respectively) instruct developing neurons to die, both in vitro and in vivo. By contrast, TrkB (also known as Ntrk2), a closely related receptor primarily expressed in the central nervous system, does not. These results indicate that TrkA and TrkC behave as dependence receptors, explaining why developing sympathetic and sensory neurons become trophic-factor-dependent for survival. We suggest that the expansion of the Trk gene family that accompanied the segregation of the peripheral from the central nervous system generated a novel mechanism of cell number control.

Date: 2010
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DOI: 10.1038/nature09336

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