Neurotrophin-evoked depolarization requires the sodium channel Nav1.9

Robert Blum, Karl W. Kafitz, Arthur Konnerth

Research output: Contribution to journalReview articlepeer-review

238 Scopus citations

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.

Original languageEnglish
Pages (from-to)687-693
Number of pages7
JournalNature
Volume419
Issue number6908
DOIs
StatePublished - 17 Oct 2002
Externally publishedYes

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