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The Journal of Neuroscience, July 11, 2007, 27(28):7597-7603; doi:10.1523/JNEUROSCI.0563-07.2007

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Cellular/Molecular
Anterograde Transport and Secretion of Brain-Derived Neurotrophic Factor along Sensory Axons Promote Schwann Cell Myelination

Benjamin K. Ng,^1 * Lian Chen,^2 * Wilhelm Mandemakers,³ José M. Cosgaya,⁴ and Jonah R. Chan¹

¹Zilkha Neurogenetic Institute, Keck School of Medicine, University of Southern California, Los Angeles, California 90033, ²National Institute of Child Health and Development, National Institutes of Health, Bethesda, Maryland 20892, ³Department of Human Genetics, Katholieke Universiteit Leuven, 3000 Leuven, Belgium, and ⁴Instituto de Investigaciones Biomedicas, Consejo Superior de Investigaciones, Cientificas and Universidad Autonoma de Madrid, 28029 Madrid, Spain

Correspondence should be addressed to Dr. Jonah R. Chan, Zilkha Neurogenetic Institute, Department of Biochemistry and Molecular Biology, Keck School of Medicine, University of Southern California, 1501 San Pablo Street, ZNI 421, Los Angeles, CA 90033. Email: jonah.chan{at}usc.edu

The neurotrophin brain-derived neurotrophic factor (BDNF) inhibits Schwann cell (SC) migration and promotes myelination via the p75 neurotrophin receptor (NTR). Despite these recent findings, the expression, localization, and mechanism of BDNF action has yet to be determined. Here we demonstrate that the sensory neurons of the dorsal root ganglion (DRG) are a major source of BDNF during postnatal development. The expression of BDNF is initially elevated before myelination and decreases dramatically after the onset of myelination. BDNF expression is controlled in part by transcriptional regulation and the increased expression of the truncated TrkB receptor on SCs. To investigate the possible mechanism of BDNF transport and release, multicompartment Campenot chambers were used. DRG neurons transported and secreted endogenous BDNF along the surface of axons in anterograde fashion. In an attempt to enhance myelination by SCs, DRG neurons were transduced with an adenovirus to overexpress BDNF. BDNF was transported and secreted along the axons and enhanced myelination when compared with control cocultures. Together, the events surrounding the expression, localization, and mechanism of BDNF action in DRG neurons may hint at potential therapeutic implications to efficiently promote remyelination.

Key words: Schwann cell; myelination; dorsal root ganglion neurons; neurotrophins; anterograde; BDNF

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Received Feb. 8, 2007; revised May 9, 2007; accepted June 5, 2007.

Correspondence should be addressed to Dr. Jonah R. Chan, Zilkha Neurogenetic Institute, Department of Biochemistry and Molecular Biology, Keck School of Medicine, University of Southern California, 1501 San Pablo Street, ZNI 421, Los Angeles, CA 90033. Email: jonah.chan{at}usc.edu

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