BMC Cancer, 2010 Background Rapid and effective treatment of cancer-induced bone pain remains a clinical challenge and patients with bone metastasis are more likely to experience severe pain.
Li Xiao-Qing +7 more
doaj +1 more source
Functional upregulation of nav1.8 sodium channels on the membrane of dorsal root Ganglia neurons contributes to the development of cancer-induced bone pain. [PDF]
PLoS ONE, 2014 We have previously reported that enhanced excitability of dorsal root ganglia (DRG) neurons contributes to the development of bone cancer pain, which severely decreases the quality of life of cancer patients.
Xiao-Dan Liu +5 more
doaj +1 more source
The parabss1 Drosophila melanogaster as Model for Chronic Nociception: Insights Into Cannabidiol Analgesic Effects. [PDF]
Eur J PainABSTRACT Background Chronic pain, which is often unrelated to ongoing injury, is poorly understood and difficult to treat. Genetic studies have identified voltage‐gated sodium (Nav) channels, particularly gain‐of‐function mutations such as L858F and R1150W in human NaV1.7, as involved in the development of chronic pain. Methods A chronic pain model was
Malta SM +7 more
europepmc +2 more sources
Deletion of Tsc2 in nociceptors reduces target innervation, ion channel expression, and sensitivity to heat [PDF]
, 2018 The mechanistic target of rapamycin complex 1 (mTORC1) is known to regulate cellular growth pathways, and its genetic activation is sufficient to enhance regenerative axon growth following injury to the central or peripheral nervous systems.
Carlin, Dan +6 more
core +2 more sources
Increased peripheral nerve excitability and local NaV1.8 mRNA up-regulation in painful neuropathy
Molecular Pain, 2009 Background Neuropathic pain caused by peripheral nerve injury is a chronic disorder that represents a significant clinical challenge because the pathological mechanisms have not been fully elucidated.
Matsuka Yoshizo +6 more
doaj +1 more source
Nav1.8, an analgesic target for nonpsychotomimetic phytocannabinoids. [PDF]
Proc Natl Acad Sci U S APain impacts billions of people worldwide, but treatment options are limited and have a spectrum of adverse effects. The search for safe and nonaddictive pain treatments has led to a focus on key mediators of nociceptor excitability. Voltage-gated sodium (Nav) channels in the peripheral nervous system—Nav1.7, Nav1.8, and Nav1.9—play crucial roles in ...
Ghovanloo MR +3 more
europepmc +3 more sources
Journal of Pharmacological Sciences, 2008 This study was conducted to determine whether Nav1.8 contributes to the release and/or synthesis of substance P (SP) in adult mice dorsal root ganglion (DRG) neurons.
He-Bin Tang +6 more
doaj +1 more source
Isoflurane Inhibits the Tetrodotoxin-resistant Voltage-gated Sodium Channel Nav1.8 [PDF]
Anesthesiology, 2009 Background Voltage-gated sodium channels (Nav) mediate neuronal action potentials. Tetrodotoxin inhibits all Nav isoforms, but Nav1.8 and Nav1.9 are relatively tetrodotoxin-resistant (TTX-r) compared to other isoforms. Nav1.8 is highly expressed in dorsal root ganglion neurons and is functionally linked to nociception, but the ...
Karl F, Herold +3 more
openaire +2 more sources
Inhibiting Nav1.8 for pain: Lessons from patients and from neurons. [PDF]
Proc Natl Acad Sci U S AWaxman SG, Vasylyev DV.
europepmc +2 more sources
Correlation of Nav1.8 and Nav1.9 sodium channel expression with neuropathic pain in human subjects with lingual nerve neuromas [PDF]
, 2013 Background: Voltage-gated sodium channels Nav1.8 and Nav1.9 are expressed preferentially in small diameter sensory neurons, and are thought to play a role in the generation of ectopic activity in neuronal cell bodies and/or their axons following ...
Alison R Loescher +8 more
core +2 more sources