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.
Originalsprache | Englisch |
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Seiten (von - bis) | 687-693 |
Seitenumfang | 7 |
Fachzeitschrift | Nature |
Jahrgang | 419 |
Ausgabenummer | 6908 |
DOIs | |
Publikationsstatus | Veröffentlicht - 17 Okt. 2002 |
Extern publiziert | Ja |