Neurotrophin-evoked depolarization requires the sodium channel NaV1.9

摘要: Brain-derived neurotrophic factor (BDNF) and other neurotrophins are essential for normal brain function. Many types of neurons in the central nervous system excited by BDNF or neurotrophin-4/5, an action that has recently been implicated synaptic plasticity. The mechanisms involved this transmitter-like remains unclear. Here, screening candidate genes with antisense messenger RNA expression approach co-expressing receptor tyrosine kinase TrkB various sodium channels, we demonstrate tetrodotoxin-insensitive channel Na(V)1.9 underlies neurotrophin-evoked excitation. These results establish molecular basis depolarization reveal a mechanism ligand-mediated activation.