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https://www.readbyqxmd.com/read/28326938/mechanisms-of-nerve-growth-factor-signaling-in-bone-nociceptors-and-in-an-animal-model-of-inflammatory-bone-pain
#1
Sara Nencini, Mitchell Ringuet, Dong-Hyun Kim, Yu-Jen Chen, Claire Greenhill, Jason J Ivanusic
Sequestration of nerve growth factor has been used successfully in the management of pain in animal models of bone disease and in human osteoarthritis. However, the mechanisms of nerve growth factor-induced bone pain and its role in modulating inflammatory bone pain remain to be determined. In this study, we show that nerve growth factor receptors (TrkA and p75) and some other nerve growth factor-signaling molecules (TRPV1 and Nav1.8, but not Nav1.9) are expressed in substantial proportions of rat bone nociceptors...
January 2017: Molecular Pain
https://www.readbyqxmd.com/read/28298301/in-vivo-optogenetic-activation-of-nav1-8-cutaneous-nociceptors-and-their-responses-to-natural-stimuli
#2
Megan L Uhelski, Daniel J Bruce, Philippe Seguela, George L Wilcox, Donald A Simone
Optogenetic methods utilizing expression of the light-sensitive protein channelrhodopsin-2 (ChR2) in neurons have enabled selective activation of specific subtypes or groups of neurons to determine their functions. Using a transgenic mouse model in which neurons natively expressing Nav1.8, a tetrodotoxin-resistant voltage-gated sodium channel, also express the light-gated channel ChR2, we have been able to determine the functional properties of Nav1.8-expressing cutaneous nociceptors of the glabrous skin in vivo...
March 15, 2017: Journal of Neurophysiology
https://www.readbyqxmd.com/read/28225079/multiple-sodium-channel-isoforms-mediate-the-pathological-effects-of-pacific-ciguatoxin-1
#3
Marco C Inserra, Mathilde R Israel, Ashlee Caldwell, Joel Castro, Jennifer R Deuis, Andrea M Harrington, Angelo Keramidas, Sonia Garcia-Caraballo, Jessica Maddern, Andelain Erickson, Luke Grundy, Grigori Y Rychkov, Katharina Zimmermann, Richard J Lewis, Stuart M Brierley, Irina Vetter
Human intoxication with the seafood poison ciguatoxin, a dinoflagellate polyether that activates voltage-gated sodium channels (NaV), causes ciguatera, a disease characterised by gastrointestinal and neurological disturbances. We assessed the activity of the most potent congener, Pacific ciguatoxin-1 (P-CTX-1), on NaV1.1-1.9 using imaging and electrophysiological approaches. Although P-CTX-1 is essentially a non-selective NaV toxin and shifted the voltage-dependence of activation to more hyperpolarising potentials at all NaV subtypes, an increase in the inactivation time constant was observed only at NaV1...
February 22, 2017: Scientific Reports
https://www.readbyqxmd.com/read/28216001/loperamide-inhibits-sodium-channels-to-alleviate-inflammatory-hyperalgesia
#4
Ying Wu, Beiyan Zou, Lingli Liang, Min Li, Yuan-Xiang Tao, Haibo Yu, Xiaoliang Wang, Min Li
Previous studies demonstrated that Loperamide, originally known as an anti-diarrheal drug, is a promising analgesic agent primarily targeting mu-opioid receptors. However some evidences suggested that non-opioid mechanisms may be contributing to its analgesic effect. In the present study, Loperamide was identified as a Nav1.7 blocker in a pilot screen. In HEK293 cells expressing Nav1.7 sodium channels, Loperamide blocked the resting state of Nav1.7 channels (IC50 = 1.86 ± 0.11 μM) dose-dependently and reversibly...
February 16, 2017: Neuropharmacology
https://www.readbyqxmd.com/read/28211895/electroacupuncture-attenuates-cfa-induced-inflammatory-pain-by-suppressing-nav1-8-through-s100b-trpv1-opioid-and-adenosine-pathways-in-mice
#5
Hsien-Yin Liao, Ching-Liang Hsieh, Chun-Ping Huang, Yi-Wen Lin
Pain is associated with several conditions, such as inflammation, that result from altered peripheral nerve properties. Electroacupuncture (EA) is a common Chinese clinical medical technology used for pain management. Using an inflammatory pain mouse model, we investigated the effects of EA on the regulation of neurons, microglia, and related molecules. Complete Freund's adjuvant (CFA) injections produced a significant mechanical and thermal hyperalgesia that was reversed by EA or a transient receptor potential V1 (TRPV1) gene deletion...
February 13, 2017: Scientific Reports
https://www.readbyqxmd.com/read/28166971/functional-and-molecular-characterization-of-voltage-gated-sodium-channel-nav-1-8-in-bull-spermatozoa
#6
Dharmendra Singh Chauhan, Dilip Kumar Swain, Nadeem Shah, Hanuman Prasad Yadav, Udayraj P Nakade, Vijay Kumar Singh, Rajesh Nigam, Sarvajeet Yadav, Satish Kumar Garg
The aim of our study was to characterize the voltage gated sodium channel Nav 1.8 in bull spermatozoa. Forty ejaculates were collected from four Hariana bulls and semen samples were pooled in view of the nonsignificant variations between different ejaculates. Functional characterization was undertaken using A-803467, a selective blocker of Nav1.8, and veratridine as an opener of the voltage gated sodium channels while molecular characterization was done using western blotting and indirect immunofluorescence assays...
March 1, 2017: Theriogenology
https://www.readbyqxmd.com/read/28162610/-368-sodium-channel-nav1-8-mediates-axonal-ttx-resistant-conduction-in-peripheral-c-fibres-in-mice
#7
A Vyshnevska, A Klein, P Reeh, M Ringkamp, M Schmelz, R Carr
No abstract text is available yet for this article.
April 2016: Journal of Pain: Official Journal of the American Pain Society
https://www.readbyqxmd.com/read/28115552/xenin-augments-duodenal-anion-secretion-via-activation-of-afferent-neural-pathways
#8
Izumi Kaji, Yasutada Akiba, Ikuo Kato, Koji Maruta, Atsukazu Kuwahara, Jonathan D Kaunitz
Xenin-25, a neurotensin (NT)-related anorexigenic gut hormone generated mostly in the duodenal mucosa, is believed to increase the rate of duodenal ion secretion, since xenin-induced diarrhea is not present after Roux-en-Y gastric bypass surgery. Since the local effects of xenin on duodenal ion secretion have remained uninvestigated, we thus examined the neural pathways underlying xenin-induced duodenal anion secretion. Intravenous infusion of xenin-8, a bioactive C-terminal fragment of xenin-25, dose-dependently increased the rate of duodenal HCO3- secretion in perfused duodenal loops of anesthetized rats...
January 23, 2017: Journal of Pharmacology and Experimental Therapeutics
https://www.readbyqxmd.com/read/28105664/visceral-and-somatic-pain-modalities-reveal-nav-1-7-independent-visceral-nociceptive-pathways
#9
James R F Hockley, Rafael González-Cano, Sheridan McMurray, Miguel A Tejada-Giraldez, Cian McGuire, Antonio Torres, Anna L Wilbrey, Vincent Cibert-Goton, Francisco R Nieto, Thomas Pitcher, Charles H Knowles, José Manuel Baeyens, John N Wood, Wendy J Winchester, David C Bulmer, Cruz Miguel Cendán, Gordon McMurray
Voltage-gated sodium channel NaV 1.7 is required for acute and inflammatory pain in mice and humans but its significance for visceral pain is unknown. Here we examine the role of NaV 1.7 in visceral pain processing and the development of referred hyperalgesia using a conditional nociceptor-specific NaV 1.7 knockout mouse (NaV 1.7(Nav1.8) ) and selective small-molecule NaV 1.7 antagonist PF-5198007. NaV 1.7(Nav1.8) mice showed normal nociceptive behaviours to intracolonic application of either capsaicin or mustard oil, stimuli known to evoke sustained nociceptor activity and sensitization following tissue damage, respectively...
January 20, 2017: Journal of Physiology
https://www.readbyqxmd.com/read/28079757/pathogenesis-of-abdominal-pain-in-bowel-obstruction-role-of-mechanical-stress-induced-upregulation-of-nerve-growth-factor-in-gut-smooth-muscle-cells
#10
You-Min Lin, Yu Fu, John Winston, Ravi Radhakrishnan, Sushil K Sarna, Li-Yen M Huang, Xuan-Zheng Shi
Abdominal pain is one of the major symptoms in bowel obstruction (BO); its cellular mechanisms remain incompletely understood. We tested the hypothesis that mechanical stress in obstruction upregulates expression of nociception mediator nerve growth factor (NGF) in gut smooth muscle cells (SMCs), and NGF sensitizes primary sensory nerve to contribute to pain in BO. Partial colon obstruction was induced with a silicon band implanted in the distal bowel of Sprague-Dawley rats. Colon-projecting sensory neurons in the dorsal root ganglia (T13 to L2) were identified for patch-clamp and gene expression studies...
April 2017: Pain
https://www.readbyqxmd.com/read/28074005/synergistic-regulation-of-serotonin-and-opioid-signaling-contributes-to-pain-insensitivity-in-nav1-7-knockout-mice
#11
Jörg Isensee, Leonhardt Krahé, Katharina Moeller, Vanessa Pereira, Jane E Sexton, Xiaohui Sun, Edward Emery, John N Wood, Tim Hucho
Genetic loss of the voltage-gated sodium channel Nav1.7 (Nav1.7(-/-)) results in lifelong insensitivity to pain in mice and humans. One underlying cause is an increase in the production of endogenous opioids in sensory neurons. We analyzed whether Nav1.7 deficiency altered nociceptive heterotrimeric guanine nucleotide-binding protein-coupled receptor (GPCR) signaling, such as initiated by GPCRs that respond to serotonin (pronociceptive) or opioids (antinociceptive), in sensory neurons. We found that the nociceptive neurons of Nav1...
January 10, 2017: Science Signaling
https://www.readbyqxmd.com/read/28069705/multilevel-analyses-of-scn5a-mutations-in-arrhythmogenic-right-ventricular-dysplasia-cardiomyopathy-suggest-non-canonical-mechanisms-for-disease-pathogenesis
#12
Anneline S J M Te Riele, Esperanza Agullo-Pascual, Cynthia A James, Alejandra Leo-Macias, Marina Cerrone, Mingliang Zhang, Xianming Lin, Bin Lin, Nara L Sobreira, Nuria Amat-Alarcon, Roos F Marsman, Brittney Murray, Crystal Tichnell, Jeroen F van der Heijden, Dennis Dooijes, Toon A B van Veen, Harikrishna Tandri, Steven J Fowler, Richard N W Hauer, Gordon Tomaselli, Maarten P van den Berg, Matthew R G Taylor, Francesca Brun, Gianfranco Sinagra, Arthur A M Wilde, Luisa Mestroni, Connie R Bezzina, Hugh Calkins, J Peter van Tintelen, Lei Bu, Mario Delmar, Daniel P Judge
AIMS: Arrhythmogenic Right Ventricular Dysplasia/Cardiomyopathy (ARVD/C) is often associated with desmosomal mutations. Recent studies suggest an interaction between the desmosome and sodium channel protein Nav1.5. We aimed to determine the prevalence and biophysical properties of mutations in SCN5A (the gene encoding Nav1.5) in ARVD/C. METHODS AND RESULTS: We performed whole-exome sequencing in six ARVD/C patients (33% male, 38.2 ± 12.1 years) without a desmosomal mutation...
January 2017: Cardiovascular Research
https://www.readbyqxmd.com/read/28035974/a-novel-toxin-from-haplopelma-lividum-selectively-inhibits-the-nav1-8-channel-and-possesses-potent-analgesic-efficacy
#13
Ping Meng, Honggang Huang, Gan Wang, Shilong Yang, Qiuming Lu, Jingze Liu, Ren Lai, Mingqiang Rong
Spider venoms are a complex mixture of peptides with a large number of neurotoxins targeting ion channels. Although thousands of peptide toxins have been identified from venoms of numerous species of spiders, many unknown species urgently need to be investigated. In this study, a novel sodium channel inhibitor, µ-TRTX-Hl1a, was identified from the venom of Haplopelma lividum. It contained eight cysteines and formed a conserved cysteine pattern of ICK motif. µ-TRTX-Hl1a inhibited the TTX-resistant (TTX-r) sodium channel current rather than the TTX-sensitive (TTX-s) sodium channel current...
December 26, 2016: Toxins
https://www.readbyqxmd.com/read/28034736/cutaneous-iontophoresis-of-%C3%AE-conotoxin-cniiic-a-potent-nav1-4-antagonist-with-analgesic-anaesthetic-and-myorelaxant-properties
#14
Sergio Del Río-Sancho, Cecile Cros, Bethsabée Coutaz, Muriel Cuendet, Yogeshvar N Kalia
Cutaneous iontophoretic delivery of μ-conotoxin CnIIIC (XEP), a potent peptide antagonist of the NaV1.4 sodium channel, was investigated using porcine ear skin and validated using human abdominal skin. Initial results demonstrated that cutaneous deposition of XEP following iontophoresis was superior to passive delivery and increased with current density. XEP deposition after iontophoresis at 0.1, 0.3 and 0.5mA/cm(2) for 2h and 4h was 22.4±0.4, 34.5±1.4, 57.4±7.6μg/cm(2) and 30.6±5.4, 53.9±17.2, 90.9±30...
December 26, 2016: International Journal of Pharmaceutics
https://www.readbyqxmd.com/read/28025109/deet-potentiates-the-development-and-persistence-of-anticholinesterase-dependent-chronic-pain-signs-in-a-rat-model-of-gulf-war-illness-pain
#15
L K Flunker, T J Nutter, R D Johnson, B Y Cooper
Exposure to DEET (N,N-diethyl-meta-toluamide) may have influenced the pattern of symptoms observed in soldiers with GWI (Gulf War Illness; Haley and Kurt, 1997). We examined how the addition of DEET (400mg/kg; 50% topical) to an exposure protocol of permethrin (2.6mg/kg; topical), chlorpyrifos (CP; 120mg/kg), and pyridostigmine bromide (PB;13mg/kg) altered the emergence and pattern of pain signs in an animal model of GWI pain (Nutter et al., 2015). Rats underwent behavioral testing before, during and after a 4week exposure: 1) hindlimb pressure withdrawal threshold; 2) ambulation (movement distance and rate); and 3) resting duration...
December 23, 2016: Toxicology and Applied Pharmacology
https://www.readbyqxmd.com/read/27989687/role-of-protein-kinase-c-in-metabolic-regulation-of-the-cardiac-na-channel
#16
Man Liu, Guangbin Shi, Kai-Chien Yang, Lianzhi Gu, Anumantha G Kanthasamy, Vellareddy Anantharam, Samuel C Dudley
BACKGROUND: The reduced form of nicotinamide adenine dinucleotide (NADH) increases in cardiomyopathy, activates protein kinase C (PKC), up-regulates mitochondrial reactive oxygen species (mitoROS), and down-regulates the cardiac Na(+) channel (NaV1.5). OBJECTIVE: The purpose of this study was to determine how NADH signals down-regulation of NaV1.5. METHODS: Isolated mouse cardiomyocytes were used for patch-clamp recording and for monitoring mitoROS with MitoSOX Red...
March 2017: Heart Rhythm: the Official Journal of the Heart Rhythm Society
https://www.readbyqxmd.com/read/27984182/contribution-of-nav1-8-sodium-channels-to-retinal-function
#17
Benjamin J Smith, Patrice D Côté, François Tremblay
We examined the contribution of the sodium channel isoform Nav1.8 to retinal function using the specific blocker A803467. We found that A803467 has little influence on the electroretinogram (ERG) a- and b-waves, but significantly reduces the oscillatory potentials (OPs) to 40-60% of their original amplitude, with significant changes in implicit time in the rod-driven range. To date, only two cell types were found in mouse to express Nav1.8; the starburst amacrine cells (SBACs), and a subtype of retinal ganglion cells (RGCs)...
January 6, 2017: Neuroscience
https://www.readbyqxmd.com/read/27916453/shank3-deficiency-impairs-heat-hyperalgesia-and-trpv1-signaling-in-primary-sensory-neurons
#18
Qingjian Han, Yong Ho Kim, Xiaoming Wang, Di Liu, Zhi-Jun Zhang, Alexandra L Bey, Mark Lay, Wonseok Chang, Temugin Berta, Yan Zhang, Yong-Hui Jiang, Ru-Rong Ji
Abnormal pain sensitivity is commonly associated with autism spectrum disorders (ASDs) and affects the life quality of ASD individuals. SHANK3 deficiency was implicated in ASD and pain dysregulation. Here, we report functional expression of SHANK3 in mouse dorsal root ganglion (DRG) sensory neurons and spinal cord presynaptic terminals. Homozygous and heterozygous Shank3 complete knockout (Δe4-22) results in impaired heat hyperalgesia in inflammatory and neuropathic pain. Specific deletion of Shank3 in Nav1...
December 21, 2016: Neuron
https://www.readbyqxmd.com/read/27905525/inhibition-of-cystathionine-%C3%AE-synthetase-suppresses-sodium-channel-activities-of-dorsal-root-ganglion-neurons-of-rats-with-lumbar-disc-herniation
#19
Jun Yan, Shufen Hu, Kang Zou, Min Xu, Qianliang Wang, Xiuhua Miao, Shan Ping Yu, Guang-Yin Xu
The pathogenesis of pain in lumbar disc herniation (LDH) remains poorly understood. We have recently demonstrated that voltage-gated sodium channels (VGSCs) in dorsal root ganglion (DRG) neurons were sensitized in a rat model of LDH. However, the detailed molecular mechanism for sensitization of VGSCs remains largely unknown. This study was designed to examine roles of the endogenous hydrogen sulfide synthesizing enzyme cystathionine β-synthetase (CBS) in sensitization of VGSCs in a previously validated rat model of LDH...
December 1, 2016: Scientific Reports
https://www.readbyqxmd.com/read/27896032/gene-expression-profile-of-sodium-channel-subunits-in-the-anterior-cingulate-cortex-during-experimental-paclitaxel-induced-neuropathic-pain-in-mice
#20
Willias Masocha
Paclitaxel, a chemotherapeutic agent, causes neuropathic pain whose supraspinal pathophysiology is not fully understood. Dysregulation of sodium channel expression, studied mainly in the periphery and spinal cord level, contributes to the pathogenesis of neuropathic pain. We examined gene expression of sodium channel (Nav) subunits by real time polymerase chain reaction (PCR) in the anterior cingulate cortex (ACC) at day 7 post first administration of paclitaxel, when mice had developed paclitaxel-induced thermal hyperalgesia...
2016: PeerJ
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