Diversity of Expression of the Sensory Neuron-Specific TTX-Resistant Voltage-Gated Sodium Ion Channels SNS and SNS2

Amaya, Fumimasa; Décosterd, Isabelle; Samad, Tarek A.; Plumpton, Christopher; Tate, Simon; Costigan, Michael; Woolf, Clifford J.

doi:10.1006/mcne.1999.0828

Cited by 261 publications

(180 citation statements)

References 35 publications

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“…All small (ϳ25 m) diameter WT DRG neurons exhibit a TTXr-Slow current, and half have a TTXr-Per current as well. We never find any neuron in WT DRG cultures with TTXr-Per but no TTXr-Slow, consistent with our finding in rats that Na v 1.9 always colocalizes with Na v 1.8 in DRG neurons but that Na v 1.8 is, in some rat DRG neurons, expressed without Na v 1.9 (Amaya et al, 2000). The activation threshold of TTXr-Per was approximately Ϫ60 mV when recording with a chloridebased internal solution, which is relatively depolarized compared with fluoridebased solutions .…”

Section: Discussionsupporting

confidence: 92%

“…Double labeling for Na v 1.9 immunohistochemistry and fluorescent in situ hybridization for the B 2 bradykinin receptor was performed using a DIG-labeled RNA probe specific for B 2 mRNA. The specificity of the Na v 1.8 and Na v 1.9 antibodies have been established previously (Amaya et al, 2000).…”

Section: Methodsmentioning

confidence: 99%

“…The second step is initiation of action potentials in the nociceptors by voltage-gated sodium channels (VGSCs). Among the 10 VGSC isoforms, two, Na v 1.8 (Akopian et al, 1996;Sangameswaran et al, 1997) and Na v 1.9 (Dib-Hajj et al, 1998;Tate et al, 1998), are expressed almost exclusively by small nociceptor primary afferent neurons (Amaya et al, 2000) and are tetrodotoxin insensitive. Na v 1.8 generates a tetrodotoxin-resistant (TTXr) current with a threshold of activation of Ϫ40 mV that inactivates slowly (TTXrSlow) (Akopian et al, 1996;Sangameswaran et al, 1997;Renganathan et al, 2002b;John et al, 2004), whereas Na v 1.9 is presumed from recordings in Na v 1.8 null mice, to produce a persistent current with a more hyperpolarized voltage dependence and ultraslow recovery from inactivation (TTXr-Per) Baker et al, 2003).…”

Section: Introductionmentioning

confidence: 99%

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

Amaya¹,

Wang²,

Costigan³

et al. 2006

J. Neurosci.

273

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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Section: Discussionsupporting

confidence: 92%

Section: Methodsmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

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

Amaya¹,

Wang²,

Costigan³

et al. 2006

J. Neurosci.

273

231

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“…Consistent with this notion, SCN5A is primarily expressed in cardiac tissue, while SCN10A and SCN11A transcripts are found in peripheral nociceptive sensory neurons (Akopian et al 1999;Dib-Hajj et al 1999a;Amaya et al 2000). SCN5A expression also occurs in central nervous system regions associated with the limbic system (Donahue et al 2000;Hartmann et al 1999).…”

Section: Scna Gene Expression In Teleosts and Mammalsmentioning

confidence: 55%

Gene Duplications and Evolution of Vertebrate Voltage-Gated Sodium Channels

Novak¹,

Jost

et al. 2006

J Mol Evol

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Abstract.Voltage-gated sodium channels underlie action potential generation in excitable tissue.To establish the evolutionary mechanisms that shaped the vertebrate sodium channel a-subunit (SCNA) gene family and their encoded Na v 1 proteins, we identified all SCNA genes in several teleost species. Molecular cloning revealed that teleosts have eight SCNA genes, comparable to the number in another vertebrate lineage, mammals.Prior phylogenetic analyses had indicated that teleosts and tetrapods share four monophyletic groups of SCNA genes and that tandem duplications selectively expanded the number of genes in two of the four mammalian groups. However, the number of genes in each group varies between teleosts and tetrapods suggesting different evolutionary histories in the two vertebrate lineages. Our findings from phylogenetic analysis and chromosomal mapping of Danio rerio genes indicate that tandem duplications are an unlikely mechanism for generation of the extant teleost SCNA genes. Instead, analysis of other closely mapped genes in D. rerio supports the hypothesis that a whole genome duplication was involved in expansion of the SCNA gene family in teleosts. Interestingly, despite their different evolutionary histories, mRNA analyses demonstrated a conservation of expression patterns for SCNA orthologues in teleosts and tetrapods, suggesting functional conservation.

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“…Tetrodotoxin-resistant voltage-dependent sodium channels Nav1.8 (SNS) and Nav1.9 (NaN or SNS2) are selectively expressed in small/medium-sized nociceptive neurons and contribute to the production of an action potential in these neurons. In addition, functional studies reveal that Nav1.8 and Nav1.9 have a specialized role in mediating pain [1,2,[15][16][17]. Thus, the level of gene expression and/or distribution of these channels may be altered in aging neurons that have lowered sensitivity.…”

Section: Introductionmentioning

confidence: 99%

Reduced thermal sensitivity and Nav1.8 and TRPV1 channel expression in sensory neurons of aged mice

Wang

Davis

Zwick³

et al. 2006

Neurobiology of Aging

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Sensory neurons in aging mammals undergo changes in anatomy, physiology and gene expression that correlate with reduced sensory perception. In this study we compared young and aged mice to identify proteins that might contribute to this loss of sensation. We first show using behavioral testing that thermal sensitivity in aged male and female mice is reduced. Expression of sodium channel (Nav1.8 and Nav1.9) and transient receptor potential vanilloid (TRPV) channels in DRG and peripheral nerves of young and old male mice was then examined. Immunoblotting and RT-PCR assays showed reduced Nav1.8 levels in aged mice. No change was measured in TRPV1 mRNA levels in DRG though TRPV1 protein appeared reduced in the DRG and peripheral nerves. The GFRα3 receptor, which binds the growth factor artemin and is expressed by TRPV1-positive neurons, was also decreased in the DRG of aged animals. These findings indicate that loss of thermal sensitivity in aging animals may result from a decreased level of TRPV1 and Nav1.8 and decreased trophic support that inhibits efficient transport of channel proteins to peripheral afferents.

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Diversity of Expression of the Sensory Neuron-Specific TTX-Resistant Voltage-Gated Sodium Ion Channels SNS and SNS2

Cited by 261 publications

References 35 publications

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

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

Gene Duplications and Evolution of Vertebrate Voltage-Gated Sodium Channels

Reduced thermal sensitivity and Nav1.8 and TRPV1 channel expression in sensory neurons of aged mice

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Diversity of Expression of the Sensory Neuron-Specific TTX-Resistant Voltage-Gated Sodium Ion Channels SNS and SNS2

Cited by 261 publications

References 35 publications

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

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

Gene Duplications and Evolution of Vertebrate Voltage-Gated Sodium Channels

Reduced thermal sensitivity and Nav1.8 and TRPV1 channel expression in sensory neurons of aged mice

Contact Info

Product

Resources

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

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