Results 21 to 30 of about 3,773 (193)

Biophysical and Pharmacological Characterization of Nav1.9 Voltage Dependent Sodium Channels Stably Expressed in HEK-293 Cells. [PDF]

open access: yesPLoS ONE, 2016
The voltage dependent sodium channel Nav1.9, is expressed preferentially in peripheral sensory neurons and has been linked to human genetic pain disorders, which makes it target of interest for the development of new pain therapeutics.
Zhixin Lin   +4 more
doaj   +1 more source

Understanding the physiological role of NaV1.9: Challenges and opportunities for pain modulation

open access: yesPharmacology & Therapeutics, 2023
Voltage-activated Na+ (NaV) channels are crucial contributors to rapid electrical signaling in the human body. As such, they are among the most targeted membrane proteins by clinical therapeutics and natural toxins. Several of the nine mammalian NaV channel subtypes play a documented role in pain or other sensory processes such as itch, touch, and ...
Brackx, Wayra   +4 more
openaire   +4 more sources

N58A Exerts Analgesic Effect on Trigeminal Neuralgia by Regulating the MAPK Pathway and Tetrodotoxin-Resistant Sodium Channel

open access: yesToxins, 2021
The primary studies have shown that scorpion analgesic peptide N58A has a significant effect on voltage-gated sodium channels (VGSCs) and plays an important role in neuropathic pain.
Chun-Li Li   +4 more
doaj   +1 more source

A Novel Spider Toxin Inhibits Fast Inactivation of the Nav1.9 Channel by Binding to Domain III and Domain IV Voltage Sensors

open access: yesFrontiers in Pharmacology, 2021
Venomous animals have evolved to produce peptide toxins that modulate the activity of voltage-gated sodium (Nav) channels. These specific modulators are powerful probes for investigating the structural and functional features of Nav channels.
Shuijiao Peng   +7 more
doaj   +1 more source

Effects of D-Serine and MK-801 on Neuropathic Pain and Functional Recovery in a Rat Model of Spinal Cord Injury [PDF]

open access: yesNeurospine, 2022
Objective Neuropathic pain is a common secondary complication of spinal cord injury (SCI). N-methyl-D-aspartate (NMDA) receptor activation is critical for hypersensitivity in neuropathic pain.
Dongwoo Yu   +8 more
doaj   +1 more source

Reduced pain sensitivity of episodic pain syndrome model mice carrying a Nav1.9 mutation by ANP-230, a novel sodium channel blocker

open access: yesHeliyon, 2023
The sodium channel Nav1.9 is expressed in the sensory neurons of small diameter dorsal root ganglia that transmit pain signals, and gain-of-function Nav1.9 mutations have been associated with both painful and painless disorders.
Hiroko Okuda   +4 more
doaj   +1 more source

Pharmacology of Heterologously Expressed Human NaV1.9 Channels [PDF]

open access: yesBiophysical Journal, 2014
The prevalence and impact of chronic pain is extensive and underscores the need to investigate the mechanisms that initiate and propagate neuronal pain signaling, and to identify new analgesic targets. Neuronal voltage-gated sodium (NaV) channels are implicated in different chronic pain disorders, including inflammatory pain.
Vanoye, Carlos G.   +2 more
openaire   +1 more source

Persistent (Na v 1.9) sodium currents in human dorsal root ganglion neurons. [PDF]

open access: yesPain
Abstract Nav1.9 is of interest to the pain community for a number of reasons, including the human mutations in the gene encoding Nav1.9, SCN11a, that are associated with both pain and loss of pain phenotypes. However, because much of what we know about the biophysical properties of Nav1.9 has been learned through the study of rodent sensory ...
Zhang X, Hartung JE, Gold MS.
europepmc   +3 more sources

Functional Analysis of Stably Expressed Human Nav1.9 [PDF]

open access: yesBiophysical Journal, 2012
The tetrodotoxin (TTX)-resistant voltage gated sodium channels, NaV1.8 and NaV1.9, are important for neuronal pain pathways. NaV1.9 (a.k.a. NaN) is preferentially expressed in nociceptive neurons of dorsal root ganglia. The role of NaV1.9 in inflammatory and neuropathic pain along with a restricted cellular localization makes it an attractive target ...
Vanoye, Carlos G.   +2 more
openaire   +1 more source

Contributions of NaV1.8 and NaV1.9 to excitability in human induced pluripotent stem-cell derived somatosensory neurons

open access: yesScientific Reports, 2021
The inhibition of voltage-gated sodium (NaV) channels in somatosensory neurons presents a promising novel modality for the treatment of pain. However, the precise contribution of these channels to neuronal excitability, the cellular correlate of pain, is
Matthew Alsaloum   +6 more
doaj   +1 more source

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