Persistent pain after spinal cord injury is maintained by primary afferent activity

Qing Yang, Zizhen Wu, Julia K. Hadden, Max A. Odem, Yan Zuo, Robyn J. Crook, Jeffrey A. Frost, Edgar T. Walters

Research output: Contribution to journalArticle

45 Citations (Scopus)

Abstract

Chronic pain caused by insults to the CNS (central neuropathic pain) is widely assumed to be maintained exclusively by central mechanisms. However, chronic hyperexcitablility occurs in primary nociceptors after spinal cord injury (SCI), suggesting that SCI pain also depends upon continuing activity of peripheral sensory neurons. The present study in rats (Rattus norvegicus) found persistent upregulation after SCI of protein, but not mRNA, for a voltage-gated Na + channel, Nav1.8, that is expressed almost exclusively in primary afferent neurons. Selectively knocking down Nav1.8 after SCI suppressed spontaneous activity in dissociated dorsal root ganglion neurons, reversed hypersensitivity of hindlimb withdrawal reflexes, and reduced ongoing pain assessed by a conditioned place preference test. These results show that activity in primary afferent neurons contributes to ongoing SCI pain.

Original languageEnglish (US)
Pages (from-to)10765-10769
Number of pages5
JournalJournal of Neuroscience
Volume34
Issue number32
DOIs
StatePublished - Aug 6 2014
Externally publishedYes

Fingerprint

Spinal Cord Injuries
Pain
Afferent Neurons
Nociceptors
Spinal Ganglia
Neuralgia
Sensory Receptor Cells
Hindlimb
Chronic Pain
Reflex
Hypersensitivity
Up-Regulation
Neurons
Messenger RNA
Proteins

Keywords

  • Chronic pain
  • Dorsal root ganglion
  • Nav1.8
  • Neuropathic pain
  • Nociceptor
  • Spinal contusion

ASJC Scopus subject areas

  • Neuroscience(all)

Cite this

Yang, Q., Wu, Z., Hadden, J. K., Odem, M. A., Zuo, Y., Crook, R. J., ... Walters, E. T. (2014). Persistent pain after spinal cord injury is maintained by primary afferent activity. Journal of Neuroscience, 34(32), 10765-10769. https://doi.org/10.1523/JNEUROSCI.5316-13.2014

Persistent pain after spinal cord injury is maintained by primary afferent activity. / Yang, Qing; Wu, Zizhen; Hadden, Julia K.; Odem, Max A.; Zuo, Yan; Crook, Robyn J.; Frost, Jeffrey A.; Walters, Edgar T.

In: Journal of Neuroscience, Vol. 34, No. 32, 06.08.2014, p. 10765-10769.

Research output: Contribution to journalArticle

Yang, Q, Wu, Z, Hadden, JK, Odem, MA, Zuo, Y, Crook, RJ, Frost, JA & Walters, ET 2014, 'Persistent pain after spinal cord injury is maintained by primary afferent activity', Journal of Neuroscience, vol. 34, no. 32, pp. 10765-10769. https://doi.org/10.1523/JNEUROSCI.5316-13.2014
Yang, Qing ; Wu, Zizhen ; Hadden, Julia K. ; Odem, Max A. ; Zuo, Yan ; Crook, Robyn J. ; Frost, Jeffrey A. ; Walters, Edgar T. / Persistent pain after spinal cord injury is maintained by primary afferent activity. In: Journal of Neuroscience. 2014 ; Vol. 34, No. 32. pp. 10765-10769.
@article{210335e3bc764517ad0e09d0ddccdbbc,
title = "Persistent pain after spinal cord injury is maintained by primary afferent activity",
abstract = "Chronic pain caused by insults to the CNS (central neuropathic pain) is widely assumed to be maintained exclusively by central mechanisms. However, chronic hyperexcitablility occurs in primary nociceptors after spinal cord injury (SCI), suggesting that SCI pain also depends upon continuing activity of peripheral sensory neurons. The present study in rats (Rattus norvegicus) found persistent upregulation after SCI of protein, but not mRNA, for a voltage-gated Na + channel, Nav1.8, that is expressed almost exclusively in primary afferent neurons. Selectively knocking down Nav1.8 after SCI suppressed spontaneous activity in dissociated dorsal root ganglion neurons, reversed hypersensitivity of hindlimb withdrawal reflexes, and reduced ongoing pain assessed by a conditioned place preference test. These results show that activity in primary afferent neurons contributes to ongoing SCI pain.",
keywords = "Chronic pain, Dorsal root ganglion, Nav1.8, Neuropathic pain, Nociceptor, Spinal contusion",
author = "Qing Yang and Zizhen Wu and Hadden, {Julia K.} and Odem, {Max A.} and Yan Zuo and Crook, {Robyn J.} and Frost, {Jeffrey A.} and Walters, {Edgar T.}",
year = "2014",
month = "8",
day = "6",
doi = "10.1523/JNEUROSCI.5316-13.2014",
language = "English (US)",
volume = "34",
pages = "10765--10769",
journal = "Journal of Neuroscience",
issn = "0270-6474",
publisher = "Society for Neuroscience",
number = "32",

}

TY - JOUR

T1 - Persistent pain after spinal cord injury is maintained by primary afferent activity

AU - Yang, Qing

AU - Wu, Zizhen

AU - Hadden, Julia K.

AU - Odem, Max A.

AU - Zuo, Yan

AU - Crook, Robyn J.

AU - Frost, Jeffrey A.

AU - Walters, Edgar T.

PY - 2014/8/6

Y1 - 2014/8/6

N2 - Chronic pain caused by insults to the CNS (central neuropathic pain) is widely assumed to be maintained exclusively by central mechanisms. However, chronic hyperexcitablility occurs in primary nociceptors after spinal cord injury (SCI), suggesting that SCI pain also depends upon continuing activity of peripheral sensory neurons. The present study in rats (Rattus norvegicus) found persistent upregulation after SCI of protein, but not mRNA, for a voltage-gated Na + channel, Nav1.8, that is expressed almost exclusively in primary afferent neurons. Selectively knocking down Nav1.8 after SCI suppressed spontaneous activity in dissociated dorsal root ganglion neurons, reversed hypersensitivity of hindlimb withdrawal reflexes, and reduced ongoing pain assessed by a conditioned place preference test. These results show that activity in primary afferent neurons contributes to ongoing SCI pain.

AB - Chronic pain caused by insults to the CNS (central neuropathic pain) is widely assumed to be maintained exclusively by central mechanisms. However, chronic hyperexcitablility occurs in primary nociceptors after spinal cord injury (SCI), suggesting that SCI pain also depends upon continuing activity of peripheral sensory neurons. The present study in rats (Rattus norvegicus) found persistent upregulation after SCI of protein, but not mRNA, for a voltage-gated Na + channel, Nav1.8, that is expressed almost exclusively in primary afferent neurons. Selectively knocking down Nav1.8 after SCI suppressed spontaneous activity in dissociated dorsal root ganglion neurons, reversed hypersensitivity of hindlimb withdrawal reflexes, and reduced ongoing pain assessed by a conditioned place preference test. These results show that activity in primary afferent neurons contributes to ongoing SCI pain.

KW - Chronic pain

KW - Dorsal root ganglion

KW - Nav1.8

KW - Neuropathic pain

KW - Nociceptor

KW - Spinal contusion

UR - http://www.scopus.com/inward/record.url?scp=84905717493&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=84905717493&partnerID=8YFLogxK

U2 - 10.1523/JNEUROSCI.5316-13.2014

DO - 10.1523/JNEUROSCI.5316-13.2014

M3 - Article

C2 - 25100607

AN - SCOPUS:84905717493

VL - 34

SP - 10765

EP - 10769

JO - Journal of Neuroscience

JF - Journal of Neuroscience

SN - 0270-6474

IS - 32

ER -