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Neurotrophin-evoked depolarization requires the sodium channel NaV1.9

Author

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  • Robert Blum

    (Institut für Physiologie, Ludwig-Maximilians-Universität München)

  • Karl W. Kafitz

    (Institut für Physiologie, Ludwig-Maximilians-Universität München)

  • Arthur Konnerth

    (Institut für Physiologie, Ludwig-Maximilians-Universität München)

Abstract

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.

Suggested Citation

  • Robert Blum & Karl W. Kafitz & Arthur Konnerth, 2002. "Neurotrophin-evoked depolarization requires the sodium channel NaV1.9," Nature, Nature, vol. 419(6908), pages 687-693, October.
    • Handle: RePEc:nat:nature:v:419:y:2002:i:6908:d:10.1038_nature01085
    DOI: 10.1038/nature01085
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