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Neurotrophin-evoked depolarization requires the sodium channel NaV1.9
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 Na(V)1.9 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.
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“Bath application of a low concentration (20 ng/ ml) of BDNF did not by itself induce spine-head enlargement (n = 30) (Fig. 4A) or inward currents (0.5 ± 1.2 pA, n = 5) (Fig. 4B) (19, 20).”
From Protein synthesis and neurotrophin-dependent structural plasticity of single dendritic spines (2008) · cites this paper as [19]
In the citing paper
“Bath application of a low concentration (20 ng/ ml) of BDNF did not by itself induce spine-head enlargement (n = 30) (Fig. 4A) or inward currents (0.5 ± 1.2 pA, n = 5) (Fig. 4B) (19, 20).”
From Protein synthesis and neurotrophin-dependent structural plasticity of single dendritic spines (2008) · cites this paper as [19]
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Research works printed but not linked: 1
- Kafitz, K. W., Lepier, A., Thoenen, H. & Konnerth, A. Saxitoxin-sensitivity of neurotrophin-induced rapid excitation and neurite growth. Pfluegers Arch. 441, R125 (2001)
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Metadata
- Authors
- Blum, R., Kafitz, K. W., & Konnerth, A.
- Affiliations
- Physiologisches Institut (DE)
- Corresponding author
- Konnerth, Arthur
- Venue
- Nature
- Published
- 2002-10
- Volume
- 419
- Issue
- 6908
- Pages
- 687-693
- ISSN
- 0028-0836 (ISSN-L)
- 1476-4687
- OpenAlex
- W2070568755
- Cited by
- 266
- References
- 45
- Citations by year
- 2026: 1 · 2025: 4 · 2024: 7 · 2023: 5 · 2022: 5 · 2021: 6 · 2020: 6 · 2019: 3 · 2018: 9 · 2017: 6 · 2016: 10 · 2015: 9 · 2014: 11 · 2013: 10 · 2012: 15
- FWCI
- 10.08
- Type
- journal article
- Language
- en
- Open access
- closed
- Licence
- www.springer.com/tdm (tdm)
- Locations
- Nature (publishedVersion)
- PubMed (publishedVersion)
- RePEc: Research Papers in Economics (submittedVersion)
- Topics
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Ion channel regulation and function
- Life Sciences › Neuroscience › Cellular and Molecular Neuroscience › Nerve injury and regeneration
- Life Sciences › Neuroscience › Sensory Systems › Ion Channels and Receptors
- Keywords
- neurotrophins, brain-derived neurotrophic factor, neurotrophin-4/5, TrkB receptor, synaptic plasticity, neuronal excitation
- MeSH terms
- Animals, Cell Line, Cells, Cultured, Cloning, Molecular, Electric Conductivity, Hippocampus, Humans, Molecular Sequence Data, Nerve Growth Factors, Neuroblastoma, Neurons, Neuropeptides, RNA, Messenger, Saxitoxin, Sodium, Sodium Channels, RNA, Antisense, Rats, Wistar, Brain-Derived Neurotrophic Factor, Receptor, trkB, Rats, NAV1.9 Voltage-Gated Sodium Channel
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