Neuropeptide y modulates c-fos protein expression in the cuneate nucleus and contributes to mechanical hypersensitivity following rat median nerve injury

Yi Ju Tsai, Chi Te Lin, Chun Ta Huang, Hsin Ying Wang, Lu Tai Tien, Seu Hwa Chen, June Horng Lue

Research output: Contribution to journalArticle

23 Citations (Scopus)

Abstract

This study sought to investigate the effects of injury-induced neuropeptide Y (NPY) on c-Fos expression in the cuneate neurons and neuropathic pain after median nerve injury. Four weeks after median nerve transection (MNT), the injured nerves stimulated at low intensity (0.1mA) expressed significantly less NPY-like immunoreactive (NPY-LI) fibers in the cuneate nucleus (CN) than those stimulated at high intensities (1.0mA and 10mA). Conversely, a significantly higher number of c-Fos-LI cells were observed in the CN in rats stimulated with 0.1mA compared to those stimulated with 1.0mA or 10mA. These results suggest that more NPY was released following low-intensity stimulation, and consequently fewer NPY-LI fibers and more c-Fos-LI cells were identified in the CN. Furthermore, the number of c-Fos-LI cells as well as the percentage of c-Fos-LI cuneothalamic projection neurons (CTNs) in the CN was markedly decreased after injection of NPY receptor antagonist along with retrograde tract-tracing method, indicating that NPY regulated c-Fos expression. In rats with median nerve chronic constriction injury (CCI), intracerebroventricular injection of NPY aggravated mechanical allodynia and low-intensity stimulus-evoked c-Fos expression, both of which were reversed by injection of NPY receptor antagonist. However, thermal hyperalgesia was not affected by injection of these two reagents. Taken together, these findings suggest that more NPY release, following low-intensity electrical stimulation of the injured nerve, significantly induces c-Fos expression in the CTNs, which possibly provide the ascending thalamic transmission of neuropathic pain signals.

Original languageEnglish
Pages (from-to)1609-1621
Number of pages13
JournalJournal of Neurotrauma
Volume26
Issue number9
DOIs
Publication statusPublished - Sep 1 2009

Fingerprint

Proto-Oncogene Proteins c-fos
Median Nerve
Neuropeptide Y
Neuropeptides
Hypersensitivity
Wounds and Injuries
Neuropeptide Y Receptors
Injections
Hyperalgesia
Neuralgia
Neurons
Constriction
Electric Stimulation

Keywords

  • C-Fos
  • Chronic constriction injury
  • Electrical stimulation
  • Neuropeptide Y
  • Transected median nerve

ASJC Scopus subject areas

  • Clinical Neurology

Cite this

Neuropeptide y modulates c-fos protein expression in the cuneate nucleus and contributes to mechanical hypersensitivity following rat median nerve injury. / Tsai, Yi Ju; Lin, Chi Te; Huang, Chun Ta; Wang, Hsin Ying; Tien, Lu Tai; Chen, Seu Hwa; Lue, June Horng.

In: Journal of Neurotrauma, Vol. 26, No. 9, 01.09.2009, p. 1609-1621.

Research output: Contribution to journalArticle

Tsai, Yi Ju ; Lin, Chi Te ; Huang, Chun Ta ; Wang, Hsin Ying ; Tien, Lu Tai ; Chen, Seu Hwa ; Lue, June Horng. / Neuropeptide y modulates c-fos protein expression in the cuneate nucleus and contributes to mechanical hypersensitivity following rat median nerve injury. In: Journal of Neurotrauma. 2009 ; Vol. 26, No. 9. pp. 1609-1621.
@article{15f9705d4da747098773014dc7d481ab,
title = "Neuropeptide y modulates c-fos protein expression in the cuneate nucleus and contributes to mechanical hypersensitivity following rat median nerve injury",
abstract = "This study sought to investigate the effects of injury-induced neuropeptide Y (NPY) on c-Fos expression in the cuneate neurons and neuropathic pain after median nerve injury. Four weeks after median nerve transection (MNT), the injured nerves stimulated at low intensity (0.1mA) expressed significantly less NPY-like immunoreactive (NPY-LI) fibers in the cuneate nucleus (CN) than those stimulated at high intensities (1.0mA and 10mA). Conversely, a significantly higher number of c-Fos-LI cells were observed in the CN in rats stimulated with 0.1mA compared to those stimulated with 1.0mA or 10mA. These results suggest that more NPY was released following low-intensity stimulation, and consequently fewer NPY-LI fibers and more c-Fos-LI cells were identified in the CN. Furthermore, the number of c-Fos-LI cells as well as the percentage of c-Fos-LI cuneothalamic projection neurons (CTNs) in the CN was markedly decreased after injection of NPY receptor antagonist along with retrograde tract-tracing method, indicating that NPY regulated c-Fos expression. In rats with median nerve chronic constriction injury (CCI), intracerebroventricular injection of NPY aggravated mechanical allodynia and low-intensity stimulus-evoked c-Fos expression, both of which were reversed by injection of NPY receptor antagonist. However, thermal hyperalgesia was not affected by injection of these two reagents. Taken together, these findings suggest that more NPY release, following low-intensity electrical stimulation of the injured nerve, significantly induces c-Fos expression in the CTNs, which possibly provide the ascending thalamic transmission of neuropathic pain signals.",
keywords = "C-Fos, Chronic constriction injury, Electrical stimulation, Neuropeptide Y, Transected median nerve",
author = "Tsai, {Yi Ju} and Lin, {Chi Te} and Huang, {Chun Ta} and Wang, {Hsin Ying} and Tien, {Lu Tai} and Chen, {Seu Hwa} and Lue, {June Horng}",
year = "2009",
month = "9",
day = "1",
doi = "10.1089/neu.2008.0642",
language = "English",
volume = "26",
pages = "1609--1621",
journal = "Journal of Neurotrauma",
issn = "0897-7151",
publisher = "Mary Ann Liebert Inc.",
number = "9",

}

TY - JOUR

T1 - Neuropeptide y modulates c-fos protein expression in the cuneate nucleus and contributes to mechanical hypersensitivity following rat median nerve injury

AU - Tsai, Yi Ju

AU - Lin, Chi Te

AU - Huang, Chun Ta

AU - Wang, Hsin Ying

AU - Tien, Lu Tai

AU - Chen, Seu Hwa

AU - Lue, June Horng

PY - 2009/9/1

Y1 - 2009/9/1

N2 - This study sought to investigate the effects of injury-induced neuropeptide Y (NPY) on c-Fos expression in the cuneate neurons and neuropathic pain after median nerve injury. Four weeks after median nerve transection (MNT), the injured nerves stimulated at low intensity (0.1mA) expressed significantly less NPY-like immunoreactive (NPY-LI) fibers in the cuneate nucleus (CN) than those stimulated at high intensities (1.0mA and 10mA). Conversely, a significantly higher number of c-Fos-LI cells were observed in the CN in rats stimulated with 0.1mA compared to those stimulated with 1.0mA or 10mA. These results suggest that more NPY was released following low-intensity stimulation, and consequently fewer NPY-LI fibers and more c-Fos-LI cells were identified in the CN. Furthermore, the number of c-Fos-LI cells as well as the percentage of c-Fos-LI cuneothalamic projection neurons (CTNs) in the CN was markedly decreased after injection of NPY receptor antagonist along with retrograde tract-tracing method, indicating that NPY regulated c-Fos expression. In rats with median nerve chronic constriction injury (CCI), intracerebroventricular injection of NPY aggravated mechanical allodynia and low-intensity stimulus-evoked c-Fos expression, both of which were reversed by injection of NPY receptor antagonist. However, thermal hyperalgesia was not affected by injection of these two reagents. Taken together, these findings suggest that more NPY release, following low-intensity electrical stimulation of the injured nerve, significantly induces c-Fos expression in the CTNs, which possibly provide the ascending thalamic transmission of neuropathic pain signals.

AB - This study sought to investigate the effects of injury-induced neuropeptide Y (NPY) on c-Fos expression in the cuneate neurons and neuropathic pain after median nerve injury. Four weeks after median nerve transection (MNT), the injured nerves stimulated at low intensity (0.1mA) expressed significantly less NPY-like immunoreactive (NPY-LI) fibers in the cuneate nucleus (CN) than those stimulated at high intensities (1.0mA and 10mA). Conversely, a significantly higher number of c-Fos-LI cells were observed in the CN in rats stimulated with 0.1mA compared to those stimulated with 1.0mA or 10mA. These results suggest that more NPY was released following low-intensity stimulation, and consequently fewer NPY-LI fibers and more c-Fos-LI cells were identified in the CN. Furthermore, the number of c-Fos-LI cells as well as the percentage of c-Fos-LI cuneothalamic projection neurons (CTNs) in the CN was markedly decreased after injection of NPY receptor antagonist along with retrograde tract-tracing method, indicating that NPY regulated c-Fos expression. In rats with median nerve chronic constriction injury (CCI), intracerebroventricular injection of NPY aggravated mechanical allodynia and low-intensity stimulus-evoked c-Fos expression, both of which were reversed by injection of NPY receptor antagonist. However, thermal hyperalgesia was not affected by injection of these two reagents. Taken together, these findings suggest that more NPY release, following low-intensity electrical stimulation of the injured nerve, significantly induces c-Fos expression in the CTNs, which possibly provide the ascending thalamic transmission of neuropathic pain signals.

KW - C-Fos

KW - Chronic constriction injury

KW - Electrical stimulation

KW - Neuropeptide Y

KW - Transected median nerve

UR - http://www.scopus.com/inward/record.url?scp=67549110197&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=67549110197&partnerID=8YFLogxK

U2 - 10.1089/neu.2008.0642

DO - 10.1089/neu.2008.0642

M3 - Article

C2 - 19456245

AN - SCOPUS:67549110197

VL - 26

SP - 1609

EP - 1621

JO - Journal of Neurotrauma

JF - Journal of Neurotrauma

SN - 0897-7151

IS - 9

ER -