The Role of Sodium Channels in Chronic Inflammatory and Neuropathic Pain

Amir, Ron; Argoff, Charles E.; Bennett, Gary J.; Cummins, Theodore R.; Durieux, Marcel E.; Gerner, Peter; Gold, Michael S.; Porreca, Frank; Strichartz, Gary R.

doi:10.1016/j.jpain.2006.01.444

Cited by 312 publications

(277 citation statements)

References 236 publications

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“…The primary group of the α-subunit is classified into Na v 1.1 to Na v 1.9 subgroups , which play various physiological roles in different organs and are potentially responsible for genetic diseases, chronic pain, epilepsy and cardiac dysrhythmia (Tan et al, 2001;Antzelevitch et al, 2005;Meisler and Kearney, 2005;Amir et al, 2006). Various models for VSSCs have been constructed; however, a mammalian VSSC has yet to be crystalized.…”

Section: Introductionmentioning

confidence: 99%

Differential binding of tetrodotoxin and its derivatives to voltage‐sensitive sodium channel subtypes (Na_v1.1 to Na_v1.7)

Tsukamoto

Chiba

Wakamori

et al. 2017

British J Pharmacology

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BACKGROUND AND PURPOSEThe development of subtype-selective ligands to inhibit voltage-sensitive sodium channels (VSSCs) has been attempted with the aim of developing therapeutic compounds. Tetrodotoxin (TTX) is a toxin from pufferfish that strongly inhibits VSSCs. Many TTX analogues have been identified from marine and terrestrial sources, although their specificity for particular VSSC subtypes has not been investigated. Herein, we describe the binding of 11 TTX analogues to human VSSC subtypes Na v 1.1-Na v 1.7. EXPERIMENTAL APPROACHEach VSSC subtype was transiently expressed in HEK293T cells. The inhibitory effects of TTX analogues on each subtype were assessed using whole-cell patch-clamp recordings.

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Section: Introductionmentioning

confidence: 99%

Differential binding of tetrodotoxin and its derivatives to voltage‐sensitive sodium channel subtypes (Na_v1.1 to Na_v1.7)

Tsukamoto

Chiba

Wakamori

et al. 2017

British J Pharmacology

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“…The conversion of high-threshold nociceptive pain to a low-threshold inflammatory pain is contributed to by peripheral sensitization of the nociceptor peripheral terminal (Levine and Reichling, 1999). Inflammatory mediators, including amines, prostanoids, kinins, purines, protons, and nerve growth factor (NGF), sensitize the nociceptor peripheral terminal by producing a reduction in the threshold of transducer channels (McCleskey and Gold, 1999;Julius and Basbaum, 2001), an increase in terminal membrane excitability (Amir et al, 2006), and insertion of receptors into the terminal membrane (Zhang et al, 2005). The high threshold of the transducers are reduced by posttranslational processing in response to activation by the inflammatory mediators of multiple intracellular signaling pathways [PKA, PKC, extracellular signalregulated kinase, phosphatidylinositol 3 (PI3) kinase, and phospholipase C] (Cesare et al, 1999;Aley et al, 2001;Bautista et al, 2006).…”

Section: Introductionmentioning

confidence: 99%

The Voltage-Gated Sodium Channel Na_v1.9 Is an Effector of Peripheral Inflammatory Pain Hypersensitivity

Amaya¹,

Wang²,

Costigan³

et al. 2006

J. Neurosci.

266

231

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We used a mouse with deletion of exons 4, 5, and 6 of the SCN11A (sodium channel, voltage-gated, type XI, ␣) gene that encodes the voltage-gated sodium channel Na v 1.9 to assess its contribution to pain. Na v 1.9 is present in nociceptor sensory neurons that express TRPV1, bradykinin B 2 , and purinergic P2X 3 receptors. In Na v 1.9 ؊/؊ mice, the non-inactivating persistent tetrodotoxin-resistant sodium TTXr-Per current is absent, whereas TTXr-Slow is unchanged. TTXs currents are unaffected by the mutation of Na v 1.9. Pain hypersensitivity elicited by intraplantar administration of prostaglandin E 2 , bradykinin, interleukin-1␤, capsaicin, and P2X 3 and P2Y receptor agonists, but not NGF, is either reduced or absent in Na v 1.9 ؊/؊ mice, whereas basal thermal and mechanical pain sensitivity is unchanged. Thermal, but not mechanical, hypersensitivity produced by peripheral inflammation (intraplanatar complete Freund's adjuvant) is substantially diminished in the null allele mutant mice, whereas hypersensitivity in two neuropathic pain models is unchanged in the Na v 1.9 ؊/؊ mice. Na v 1.9 is, we conclude, an effector of the hypersensitivity produced by multiple inflammatory mediators on nociceptor peripheral terminals and therefore plays a key role in mediating peripheral sensitization.

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“…Mutation in the SCN9A gene that encodes the Nav 1.7 sodium channel subtype creates two different phenotypes. People with this mutation either cannot feel the pain or have chronic familial pain syndrome (40). Reimann et al (41) carried out studies on single nucleotide polymorphism (SNP) rs6746030 and determined that it changes pain sensitivity and pain experience in common diseases, such as osteoarthritis and spinal nerve root pain.…”

Section: Discussionmentioning

confidence: 99%

The effects of bupivacaine combined with different adjuvants on block onset and duration and on ion channel expressions (SCN9A, TRPM) in sciatic nerve block in rats

Dolu¹,

Şahin

Kaplan

et al. 2016

Turk J Med Sci

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The Role of Sodium Channels in Chronic Inflammatory and Neuropathic Pain

Cited by 312 publications

References 236 publications

Differential binding of tetrodotoxin and its derivatives to voltage‐sensitive sodium channel subtypes (Na_v1.1 to Na_v1.7)

Differential binding of tetrodotoxin and its derivatives to voltage‐sensitive sodium channel subtypes (Na_v1.1 to Na_v1.7)

The Voltage-Gated Sodium Channel Na_v1.9 Is an Effector of Peripheral Inflammatory Pain Hypersensitivity

The effects of bupivacaine combined with different adjuvants on block onset and duration and on ion channel expressions (SCN9A, TRPM) in sciatic nerve block in rats

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The Role of Sodium Channels in Chronic Inflammatory and Neuropathic Pain

Cited by 312 publications

References 236 publications

Differential binding of tetrodotoxin and its derivatives to voltage‐sensitive sodium channel subtypes (Nav1.1 to Nav1.7)

Differential binding of tetrodotoxin and its derivatives to voltage‐sensitive sodium channel subtypes (Nav1.1 to Nav1.7)

The Voltage-Gated Sodium Channel Nav1.9 Is an Effector of Peripheral Inflammatory Pain Hypersensitivity

The effects of bupivacaine combined with different adjuvants on block onset and duration and on ion channel expressions (SCN9A, TRPM) in sciatic nerve block in rats

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Product

Resources

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Differential binding of tetrodotoxin and its derivatives to voltage‐sensitive sodium channel subtypes (Na_v1.1 to Na_v1.7)

Differential binding of tetrodotoxin and its derivatives to voltage‐sensitive sodium channel subtypes (Na_v1.1 to Na_v1.7)

The Voltage-Gated Sodium Channel Na_v1.9 Is an Effector of Peripheral Inflammatory Pain Hypersensitivity