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The Journal of Neuroscience, October 28, 2009, 29(43):13640-13648; doi:10.1523/JNEUROSCI.1133-09.2009

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Cellular/Molecular
Progressive Postnatal Motoneuron Loss in Mice Lacking GDF-15

Jens Strelau,¹ Adam Strzelczyk,¹ Patricia Rusu,¹ Gerald Bendner,¹ Stefan Wiese,⁵ Francesca Diella,² Amy L. Altick,³ Christopher S. von Bartheld,³ Rüdiger Klein,⁴ Michael Sendtner,⁵ and Klaus Unsicker^1,6

¹Neuroanatomy and Interdisciplinary Center for Neurosciences, University of Heidelberg, D-69120 Heidelberg, Germany, ²European Molecular Biology Laboratory Heidelberg, D-69117 Heidelberg, Germany, ³Department of Physiology and Cell Biology, University of Nevada School of Medicine, Reno, Nevada 89557, ⁴Department of Molecular Neurobiology, Max Planck Institute of Neurobiology, D-82152 Martinsried, Germany, ⁵Clinical Neurobiology, University of Würzburg, D-97078 Würzburg, Germany, and ⁶Institute of Anatomy and Cell Biology, Department of Molecular Embryology, University of Freiburg, D-79104 Freiburg, Germany

Correspondence should be addressed to Klaus Unsicker, Institute of Anatomy and Cell Biology, Department of Molecular Embryology, University of Freiburg, Albertstrasse 17, D-79104 Freiburg, Germany. E-mail: Email: ku39{at}anat.uni-freiburg

Growth/differentiation factor-15 (GDF-15) is a widely expressed distant member of the TGF-β superfamily with prominent neurotrophic effects on midbrain dopaminergic neurons. We show here that GDF-15-deficient mice exhibit progressive postnatal losses of spinal, facial, and trigeminal motoneurons. This deficit reaches a 20% maximum at 6 months and is accompanied by losses of motor axons and significant impairment of rotarod skills. Similarly, sensory neurons in dorsal root ganglia (L4, L5) are reduced by 20%, whereas sympathetic neurons are not affected. GDF-15 is expressed and secreted by Schwann cells, retrogradely transported along adult sciatic nerve axons, and promotes survival of axotomized facial neurons as well as cultured motor, sensory, and sympathetic neurons. Despite striking similarities in the GDF-15 and CNTF knock-out phenotypes, expression levels of CNTF and other neurotrophic factors in the sciatic nerve were unaltered suggesting that GDF-15 is a genuine novel trophic factor for motor and sensory neurons.

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Received Feb. 24, 2009; revised July 1, 2009; accepted July 29, 2009.

Correspondence should be addressed to Klaus Unsicker, Institute of Anatomy and Cell Biology, Department of Molecular Embryology, University of Freiburg, Albertstrasse 17, D-79104 Freiburg, Germany. E-mail: Email: ku39{at}anat.uni-freiburg

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