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J. Biol. Chem., Vol. 282, Issue 8, 5152-5159, February 23, 2007

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A Critical Role for System A Amino Acid Transport in the Regulation of Dendritic Development by Brain-derived Neurotrophic Factor (BDNF)^*

Julia Burkhalter, Hubert Fiumelli, Jeffrey D. Erickson, and Jean-Luc Martin^¶1

From the Department of Physiology, University of Lausanne, Rue du Bugnon 7, CH-1005 Lausanne, Switzerland, the Neuroscience Center, Louisiana State University Health Sciences Center, New Orleans, Louisiana 70112, and the ^¶Center for Psychiatric Neuroscience, Department of Psychiatry, University of Lausanne, Route de Cery, CH-1008 Prilly-Lausanne, Switzerland

Dendritic development is essential for the establishment of a functional nervous system. Among factors that control dendritic development, brain-derived neurotrophic factor (BDNF) has been shown to regulate dendritic length and complexity of cortical neurons. However, the cellular and molecular mechanisms that underlie these effects remain poorly understood. In this study, we examined the role of amino acid transport in mediating the effects of BDNF on dendritic development. We show that BDNF increases System A amino acid transport in cortical neurons by selective up-regulation of the sodium-coupled neutral amino acid transporter (SNAT)1. Up-regulation of SNAT1 expression and System A activity is required for the effects of BDNF on dendritic growth and branching of cortical neurons. Further analysis revealed that induction of SNAT1 expression and System A activity by BDNF is necessary in particular to enhance synthesis of tissue-type plasminogen activator, a protein that we demonstrate to be essential for the effects of BDNF on cortical dendritic morphology. Together, these data reveal that stimulation of neuronal differentiation by BDNF requires the up-regulation of SNAT1 expression and System A amino acid transport to meet the increased metabolic demand associated with the enhancement of dendritic growth and branching.

Received for publication, September 5, 2006 , and in revised form, December 14, 2006.

^* This work was supported by Swiss National Science Foundation Grant 3200BO-103652 (to J.-L. M.). The costs of publication of this article were defrayed in part by the payment of page charges. This article must therefore be hereby marked "advertisement" in accordance with 18 U.S.C. Section 1734 solely to indicate this fact.

¹ To whom correspondence should be addressed. Tel.: 41-216925556; Fax: 41-216925595; E-mail: jean-luc.martin{at}unil.ch.

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