Pain without nociceptors? Nav1.7-independent pain mechanisms

Research output: Contribution to journal › Journal article › Research › peer-review

Standard

Pain without nociceptors? Nav1.7-independent pain mechanisms. / Minett, Michael S; Falk, Sarah; Santana-Varela, Sonia; Bogdanov, Yury D; Nassar, Mohammed A; Heegaard, Anne-Marie; Wood, John N.

In: Cell Reports, Vol. 6, No. 2, 30.01.2014, p. 245-246.

Research output: Contribution to journal › Journal article › Research › peer-review

Harvard

Minett, MS, Falk, S, Santana-Varela, S, Bogdanov, YD, Nassar, MA, Heegaard, A-M & Wood, JN 2014, 'Pain without nociceptors? Nav1.7-independent pain mechanisms', Cell Reports, vol. 6, no. 2, pp. 245-246. https://doi.org/10.1016/j.celrep.2013.12.033

APA

Minett, M. S., Falk, S., Santana-Varela, S., Bogdanov, Y. D., Nassar, M. A., Heegaard, A-M., & Wood, J. N. (2014). Pain without nociceptors? Nav1.7-independent pain mechanisms. Cell Reports, 6(2), 245-246. https://doi.org/10.1016/j.celrep.2013.12.033

Vancouver

Minett MS, Falk S, Santana-Varela S, Bogdanov YD, Nassar MA, Heegaard A-M et al. Pain without nociceptors? Nav1.7-independent pain mechanisms. Cell Reports. 2014 Jan 30;6(2):245-246. https://doi.org/10.1016/j.celrep.2013.12.033

Author

Minett, Michael S ; Falk, Sarah ; Santana-Varela, Sonia ; Bogdanov, Yury D ; Nassar, Mohammed A ; Heegaard, Anne-Marie ; Wood, John N. / Pain without nociceptors? Nav1.7-independent pain mechanisms. In: Cell Reports. 2014 ; Vol. 6, No. 2. pp. 245-246.

Bibtex

@article{b630c631248542308a055ee5e8390d67,
title = "Pain without nociceptors?: Nav1.7-independent pain mechanisms",
abstract = "Nav1.7, a peripheral neuron voltage-gated sodium channel, is essential for pain and olfaction in mice and humans. We examined the role of Nav1.7 as well as Nav1.3, Nav1.8, and Nav1.9 in different mouse models of chronic pain. Constriction-injury-dependent neuropathic pain is abolished when Nav1.7 is deleted in sensory neurons, unlike nerve-transection-related pain, which requires the deletion of Nav1.7 in sensory and sympathetic neurons for pain relief. Sympathetic sprouting that develops in parallel with nerve-transection pain depends on the presence of Nav1.7 in sympathetic neurons. Mechanical and cold allodynia required distinct sets of neurons and different repertoires of sodium channels depending on the nerve injury model. Surprisingly, pain induced by the chemotherapeutic agent oxaliplatin and cancer-induced bone pain do not require the presence of Nav1.7 sodium channels or Nav1.8-positive nociceptors. Thus, similar pain phenotypes arise through distinct cellular and molecular mechanisms. Therefore, rational analgesic drug therapy requires patient stratification in terms of mechanisms and not just phenotype.",
author = "Minett, {Michael S} and Sarah Falk and Sonia Santana-Varela and Bogdanov, {Yury D} and Nassar, {Mohammed A} and Anne-Marie Heegaard and Wood, {John N}",
note = "Copyright {\textcopyright} 2014 The Authors. Published by Elsevier Inc. All rights reserved.",
year = "2014",
month = jan,
day = "30",
doi = "10.1016/j.celrep.2013.12.033",
language = "English",
volume = "6",
pages = "245--246",
journal = "Cell Reports",
issn = "2211-1247",
publisher = "Cell Press",
number = "2",

}

RIS

TY - JOUR

T1 - Pain without nociceptors?

T2 - Nav1.7-independent pain mechanisms

AU - Minett, Michael S

AU - Falk, Sarah

AU - Santana-Varela, Sonia

AU - Bogdanov, Yury D

AU - Nassar, Mohammed A

AU - Heegaard, Anne-Marie

AU - Wood, John N

N1 - Copyright © 2014 The Authors. Published by Elsevier Inc. All rights reserved.

PY - 2014/1/30

Y1 - 2014/1/30

N2 - Nav1.7, a peripheral neuron voltage-gated sodium channel, is essential for pain and olfaction in mice and humans. We examined the role of Nav1.7 as well as Nav1.3, Nav1.8, and Nav1.9 in different mouse models of chronic pain. Constriction-injury-dependent neuropathic pain is abolished when Nav1.7 is deleted in sensory neurons, unlike nerve-transection-related pain, which requires the deletion of Nav1.7 in sensory and sympathetic neurons for pain relief. Sympathetic sprouting that develops in parallel with nerve-transection pain depends on the presence of Nav1.7 in sympathetic neurons. Mechanical and cold allodynia required distinct sets of neurons and different repertoires of sodium channels depending on the nerve injury model. Surprisingly, pain induced by the chemotherapeutic agent oxaliplatin and cancer-induced bone pain do not require the presence of Nav1.7 sodium channels or Nav1.8-positive nociceptors. Thus, similar pain phenotypes arise through distinct cellular and molecular mechanisms. Therefore, rational analgesic drug therapy requires patient stratification in terms of mechanisms and not just phenotype.

AB - Nav1.7, a peripheral neuron voltage-gated sodium channel, is essential for pain and olfaction in mice and humans. We examined the role of Nav1.7 as well as Nav1.3, Nav1.8, and Nav1.9 in different mouse models of chronic pain. Constriction-injury-dependent neuropathic pain is abolished when Nav1.7 is deleted in sensory neurons, unlike nerve-transection-related pain, which requires the deletion of Nav1.7 in sensory and sympathetic neurons for pain relief. Sympathetic sprouting that develops in parallel with nerve-transection pain depends on the presence of Nav1.7 in sympathetic neurons. Mechanical and cold allodynia required distinct sets of neurons and different repertoires of sodium channels depending on the nerve injury model. Surprisingly, pain induced by the chemotherapeutic agent oxaliplatin and cancer-induced bone pain do not require the presence of Nav1.7 sodium channels or Nav1.8-positive nociceptors. Thus, similar pain phenotypes arise through distinct cellular and molecular mechanisms. Therefore, rational analgesic drug therapy requires patient stratification in terms of mechanisms and not just phenotype.

U2 - 10.1016/j.celrep.2013.12.033

DO - 10.1016/j.celrep.2013.12.033

M3 - Journal article

C2 - 24440715

VL - 6

SP - 245

EP - 246

JO - Cell Reports

JF - Cell Reports

SN - 2211-1247

IS - 2

ER -

ID: 96626078