ArticleThe Journal of general physiology2008
NGF inhibits M/KCNQ currents and selectively alters neuronal excitability in subsets of sympathetic neurons depending on their M/KCNQ current background.
Article in The Journal of general physiology, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.
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Who cites it
19 citing papers in PubMed, 42 citations in OpenAlex.
- Heightened sympathetic neuron activity and altered cardiomyocyte properties in spontaneously hypertensive rats during the postnatal period.Frontiers in synaptic neuroscience · 2022Article
- Downregulation of M Current Is Coupled to Membrane Excitability in Sympathetic Neurons Before the Onset of Hypertension.Hypertension (Dallas, Tex. : 1979) · 2020Article
- KFrontiers in cellular neuroscience · 2020Review
- Inhibition of M/KFrontiers in molecular neuroscience · 2020Article
- Ethanol Elevates Excitability of Superior Cervical Ganglion Neurons by Inhibiting Kv7 Channels in a Cell Type-Specific and PI(4,5)PInternational journal of molecular sciences · 2019Article
- Article
- Noise-induced hearing loss: Neuropathic pain via Ntrk1 signaling.Molecular and cellular neurosciences · 2016Article
- Redox and nitric oxide-mediated regulation of sensory neuron ion channel function.Antioxidants & redox signaling · 2015Review
- Virtual leak channels modulate firing dynamics and synaptic integration in rat sympathetic neurons: implications for ganglionic transmission in vivo.The Journal of physiology · 2015Article
- Forskolin suppresses delayed-rectifier K+ currents and enhances spike frequency-dependent adaptation of sympathetic neurons.PloS one · 2015Article
- Opening paths to novel analgesics: the role of potassium channels in chronic pain.Trends in neurosciences · 2014Review
- Article
- Triple cysteine module within M-type K+ channels mediates reciprocal channel modulation by nitric oxide and reactive oxygen species.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2013Article
- Article
- Cholesterol inhibits M-type K+ channels via protein kinase C-dependent phosphorylation in sympathetic neurons.The Journal of biological chemistry · 2010Article
- Depolarization increases phosphatidylinositol (PI) 4,5-bisphosphate level and KCNQ currents through PI 4-kinase mechanisms.The Journal of biological chemistry · 2010Article
- Neurotrophins and target interactions in the development and regulation of sympathetic neuron electrical and synaptic properties.Autonomic neuroscience : basic & clinical · 2009Review
- p75 and TrkA signaling regulates sympathetic neuronal firing patterns via differential modulation of voltage-gated currents.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2009Article
- Enhancing m currents: a way out for neuropathic pain?Frontiers in molecular neuroscience · 2009Article
Corrections and comments
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Authors and funding
7 authors at 3 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
M/KCNQ currents play a critical role in the determination of neuronal excitability. Many neurotransmitters and peptides modulate M/KCNQ current and neuronal excitability through their G protein-coupled receptors. Nerve growth factor (NGF) activates its receptor, a member of receptor tyrosine kinase (RTK) superfamily, and crucially modulates neuronal cell survival, proliferation, and differentiation. In this study, we studied the effect of NGF on the neuronal (rat superior cervical ganglion, SCG) M/KCNQ currents and excitability. As reported before, subpopulation SCG neurons with distinct firing properties could be classified into tonic, phasic-1, and phasic-2 neurons. NGF inhibited M/KCNQ currents by similar proportion in all three classes of SCG neurons but increased the excitability only significantly in tonic SCG neurons. The effect of NGF on excitability correlated with a smaller M-current density in tonic neurons. The present study indicates that NGF is an M/KCNQ channel modulator and the characteristic modulation of the neuronal excitability by NGF may have important physiological implications.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the Socratic graph.