2017
DOI: 10.1111/bph.13962
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Abstract: This article is part of a themed section on Recent Advances in Targeting Ion Channels to Treat Chronic Pain. To view the other articles in this section visit http://onlinelibrary.wiley.com/doi/10.1111/bph.v175.12/issuetoc.

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Cited by 74 publications
(84 citation statements)
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“…The recent discovery that Na V 1.1 and 1.3 channels are involved in pain pathways (Cardoso & Lewis, 2018;Chen et al, 2014;Osteen et al, 2016) and that the Na V 1.2 channel is only located in the CNS (de Lera Ruiz & Kraus, 2015) does not impair further development of CyrTx-1a as a potential antinociceptive agent to access only peripheral Na V channel subtypes. The recent discovery that Na V 1.1 and 1.3 channels are involved in pain pathways (Cardoso & Lewis, 2018;Chen et al, 2014;Osteen et al, 2016) and that the Na V 1.2 channel is only located in the CNS (de Lera Ruiz & Kraus, 2015) does not impair further development of CyrTx-1a as a potential antinociceptive agent to access only peripheral Na V channel subtypes.…”
Section: In Vivo Toxicity Of Cyrtx-1a Compared To Hwtx-iv In Micementioning
confidence: 99%
See 1 more Smart Citation
“…The recent discovery that Na V 1.1 and 1.3 channels are involved in pain pathways (Cardoso & Lewis, 2018;Chen et al, 2014;Osteen et al, 2016) and that the Na V 1.2 channel is only located in the CNS (de Lera Ruiz & Kraus, 2015) does not impair further development of CyrTx-1a as a potential antinociceptive agent to access only peripheral Na V channel subtypes. The recent discovery that Na V 1.1 and 1.3 channels are involved in pain pathways (Cardoso & Lewis, 2018;Chen et al, 2014;Osteen et al, 2016) and that the Na V 1.2 channel is only located in the CNS (de Lera Ruiz & Kraus, 2015) does not impair further development of CyrTx-1a as a potential antinociceptive agent to access only peripheral Na V channel subtypes.…”
Section: In Vivo Toxicity Of Cyrtx-1a Compared To Hwtx-iv In Micementioning
confidence: 99%
“…The recent discovery that Na V 1.1 and 1.3 channels are involved in pain pathways (Cardoso & Lewis, 2018;Chen et al, 2014;Osteen et al, 2016) and that the Na V 1.2 channel is only located in the CNS (de Lera Ruiz & Kraus, 2015) does not impair further development of CyrTx-1a as a potential antinociceptive agent to access only peripheral Na V channel subtypes. In agreement, no central side effect was detected when the toxin was locally injected to mice for studying its action on neuromuscular system and on heat and tactile sensitivity, in vivo.…”
Section: Effects Of Cyrtx-1a Compared To Hwtx-iv On the Mouse Neumentioning
confidence: 99%
“…P2X3, Bernier et al ., ) and acid‐sensing ion channels (in particular ASIC3; Deval and Lingueglia, ). Channels expressed in nociceptors with a role in controlling sensory neuron excitability include the voltage‐gated Na + channel subtypes Na V 1.1, Na V 1.3, Na V 1.6, Na V 1.7, Na V 1.8 and Na V 1.9 (Cardoso and Lewis, ); Ca V 3 voltage‐gated Ca 2+ channel isoforms (François et al ., ) and K + channels such as two‐pore‐domain (K2P) TREK and TRESK (Mathie and Veale, ) and KCNQ (Kv7) M channels (Du et al ., ). Channels such as Ca v 2.2 (Patel et al ., ) and associated α2δ auxiliary subunits (Gong et al ., ) have a key role in regulating neurotransmitter and neuropeptide release at central terminals in the dorsal horn of the spinal cord.…”
Section: Measuring Ion Channel Function In Nociceptive Pathwaysmentioning
confidence: 99%
“…Current research activity focussed on targeting ion channels involved in pain transduction, axonal conduction and neurotransmitter release (in spinal cord through to higher centres) provides important targets for discovery of new analgesics. For example, knowledge of voltage‐gated ion channel function, such as Na channels (Cardoso and Lewis, ) and K channels (Du et al ., ) classically involved in neuronal excitability and Ca channels (Patel et al ., ) responsible for transmitter release, has progressed via advances in, amongst others, measurement of protein up‐regulation during pain states, knowledge of channel dysfunction in pain syndromes associated with human genetics and development of transgenic knock‐down and knock‐in technology to support in vitro and in vivo models. Alongside this, increased structural and functional knowledge of transient receptor potential (TRP) channels (Moran and Szallasi, ) and acid‐sensitive ion channels (ASICs) (Lee et al ., ) has generated further potential targets.…”
Section: Introductionmentioning
confidence: 99%
“…[1,2] Clarification of the structure of Na V is hampered by difficulty in crystallization, although am odel structure of Na V developed by X-ray analysis of potassium channels tructure has been proposed based on the amino acid sequence homology between these channels. [5,6] Since diseases such as epilepsy, pain and heart disease are associatedw ith particulars ubtypes, there is considerable interest in developing Na V subtype-specific modulators, and a number of peptide-derived [7] and sulfonamide-basedl igands [8] have been reported. Na V 1.1-1.4, 1.6 and 1.7, show high sensitivity to TTX (TTX-s), whereas Na V 1.5, 1.8, and 1.9 are only blocked by high concentrations of TTX (TTXr).…”
Section: Introductionmentioning
confidence: 99%