Results 171 to 180 of about 8,067 (198)

Functional and distinct roles of Piezo2-mediated mechanotransduction in dental primary afferent neurons. [PDF]

Int J Oral Sci
Lee PR, Lee K, Park JM, Kim S, Oh SB.
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Pathogenic mutations perturb calmodulin regulation of Nav1.8 channel

Biochemical and Biophysical Research Communications, 2020
The voltage-gated sodium channels play a key role in the generation and propagation of the cardiac action potential. Emerging data indicate that the Nav1.8 channel, encoded by the SCN10A gene, is a modulator of cardiac conduction and variation in the gene has been associated with arrhythmias such as atrial fibrillation (AF) and Brugada syndrome (BrS ...
Liang Hong, Meihong Zhang, Arvind Sridhar, Dawood Darbar   +3 more
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Prefrontal cortex pyramidal neurons express functional Nav1.8 tetrodotoxin‐resistant sodium currents

Clinical and Experimental Pharmacology and Physiology, 2021
AbstractIt has been repeatedly proved that Nav1.8 tetrodotoxin (TTX)‐resistant sodium currents are expressed in peripheral sensory neurons where they play important role in nociception. There are very few publications that show the presence of TTX‐resistant sodium currents in central neurons. The aim of this study was to assess if functional Nav1.8 TTX‐
Bartłomiej, Szulczyk, Michał, Pasierski, Maciej, Gawlak   +2 more
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Fenamates inhibit human sodium channel Nav1.7 and Nav1.8

Neuroscience Letters, 2019
Fenamates are N-substituted anthranilic acid derivatives, clinically used as nonsteroidal anti-inflammatory drugs (NSAIDs) in fever, pain and inflammation treatments. Previous studies have shown that they are also modulators of diverse ion channels, exhibiting either activation or inhibitory effects.
Jian-Fang, Sun, Yi-Jia, Xu, Xiao-Hua, Kong, Yang, Su, Zhan-You, Wang   +4 more
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Use-Dependent Relief of Inhibition of Nav1.8 Channels by A-887826

Molecular Pharmacology, 2023
Sodium channel inhibitors used as local anesthetics, antiarrhythmics, or antiepileptics typically have the property of use-dependent inhibition, whereby inhibition is enhanced by repetitive channel activation. For targeting pain, Nav1.8 channels are an attractive target because they are prominent in primary pain-sensing neurons, with little or no ...
Sooyeon Jo, Han-Xiong Bear Zhang, Bruce P. Bean   +2 more
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Functional and pharmacological properties of human and rat NaV1.8 channels

Neuropharmacology, 2009
The aim of this work is to characterise the functional properties of human and rat Na(V)1.8 channels and to investigate the action of anti-nociceptive agents. Na(V)1.8 alpha-subunits were expressed in mammalian sensory neuron-derived ND7/23 cells, and sodium currents were recorded using whole-cell patch clamp.
Browne, Liam E., Clare, Jeff J., Wray, Dennis   +2 more
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Analysis of human Nav1.8 expressed in SH-SY5Y neuroblastoma cells

European Journal of Pharmacology, 2005
The tetrodotoxin-resistant voltage-gated sodium channel alpha-subunit Nav1.8 is expressed in nociceptors and has been implicated in chronic pain. Difficulties of heterologous expression have so far precluded analysis of the pharmacological properties of human Nav1.8.
Lodewijk V, Dekker, Zoe, Daniels, Caroline, Hick, Kathryn, Elsegood, Sarah, Bowden, Tadge, Szestak, J Russell, Burley, Andy, Southan, David, Cronk, Iain F, James   +9 more
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Drug discovery targeting Nav1.8: Structural insights and therapeutic potential

Current Opinion in Chemical Biology
Voltage-gated sodium (Nav) channels are crucial in transmitting action potentials in neurons. The tetrodotoxin-resistant subtype Nav1.8 is predominantly expressed in the peripheral nervous system, offering a unique opportunity to design selective inhibitors for pain relief. A number of compounds have been reported to specifically block Nav1.8.
Huan, Wang, Jian, Huang, Jie, Zang, Xueqin, Jin, Nieng, Yan   +4 more
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NaV1.8 as a drug target for pain

2005
Pain is a complex phenomenon which involves central as well as peripheral neuronal mechanisms. Increased sensitivity and excitability of peripheral nociceptive neurons continues to be regarded as an important contributory event to the onset and/or maintenance of the pain state.
Lodewijk V. Dekker, David Cronk
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