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Nature 419, 687-693 (17 October 2002) | doi:10.1038/nature01085; Received 29 April 2002; Accepted 13 August 2002

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Neurotrophin-evoked depolarization requires the sodium channel NaV1.9

Robert Blum1,2, Karl W. Kafitz1,2 & Arthur Konnerth1

  1. Institut für Physiologie, Ludwig-Maximilians-Universität München, D-80336 München, Germany
  2. These authors contributed equally to this work

Correspondence to: Arthur Konnerth1 Correspondence and requests for materials should be addressed to A.K. (e-mail: Email: konnerth@lrz.uni-muenchen.de). The sequence of NaV1.9 has been deposited in the EMBL/GenBank database under accession number AJ417790.

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Brain-derived neurotrophic factor (BDNF) and other neurotrophins are essential for normal brain function. Many types of neurons in the central nervous system are excited by BDNF or neurotrophin-4/5, an action that has recently been implicated in synaptic plasticity. The mechanisms involved in this transmitter-like action of neurotrophins remains unclear. Here, by screening candidate genes with an antisense messenger RNA expression approach and by co-expressing the receptor tyrosine kinase TrkB and various sodium channels, we demonstrate that the tetrodotoxin-insensitive sodium channel NaV1.9 underlies the neurotrophin-evoked excitation. These results establish the molecular basis of neurotrophin-evoked depolarization and reveal a mechanism of ligand-mediated sodium channel activation.

  1. Institut für Physiologie, Ludwig-Maximilians-Universität München, D-80336 München, Germany
  2. These authors contributed equally to this work

Correspondence to: Arthur Konnerth1 Correspondence and requests for materials should be addressed to A.K. (e-mail: Email: konnerth@lrz.uni-muenchen.de). The sequence of NaV1.9 has been deposited in the EMBL/GenBank database under accession number AJ417790.