Involvement of the periaqueductal gray in the effect of motor cortexstimulation

Ruei Jen Chiou, Chen Wei Chang, Chung Chih Kuo

Research output: Contribution to journalArticle

14 Citations (Scopus)

Abstract

Several clinical and animal studies of different pain models reported that motor cortex stimulation (MCS) has an antinociceptive effect. In our previous study, the response of the primary somatosensory cortex (SI) to peripheral stimuli decreased after MCS. The aim of the present study was to investigate involvement of the periaqueductal gray (PAG) in this inhibitory effect of MCS. Responses of the SI to electrical stimuli applied to both forepaws of anesthetized rats were monitored to evaluate the effect of MCS. After sensory-evoked potentials (SEPs) were stable, either saline, opioid, or dopamine receptor antagonists were locally microinjected into the PAG. After drug or saline administration, MCS was applied to the forepaw area of the right motor cortex. SEPs after MCS were compared to those before MCS. In the saline group, SEPs ipsilateral to MCS decreased, but SEPs contralateral to MCS did not. The decrease in SEPs was prevented by pretreatment of the PAG with naloxone. Application of a nonspecific dopamine receptor antagonist (α-flupenthixol) to the PAG also blocked the inhibition of SEPs after MCS. Inhibition of SEPs after MCS was blocked by local application of a D1 antagonist (SCH-23390) in the PAG, but not by a D2 antagonist (eticlopride). These results suggest that the PAG participates in the inhibitory effect of MCS, and this effect of MCS may be mediated by opioid and dopamine D1 receptors within thePAG.

Original languageEnglish
Pages (from-to)28-35
Number of pages8
JournalBrain Research
Volume1500
DOIs
Publication statusPublished - Mar 15 2013

Fingerprint

Periaqueductal Gray
Motor Cortex
Evoked Potentials
eticlopride
Dopamine Antagonists
Flupenthixol
Dopamine D1 Receptors
Somatosensory Cortex
Narcotic Antagonists
Naloxone
Opioid Analgesics

Keywords

  • Antinociception
  • Dopamine
  • Electrophysiology
  • Endogenous opioid
  • Pain modulation
  • Sensory-evoked potential

ASJC Scopus subject areas

  • Neuroscience(all)
  • Clinical Neurology
  • Developmental Biology
  • Molecular Biology

Cite this

Involvement of the periaqueductal gray in the effect of motor cortexstimulation. / Chiou, Ruei Jen; Chang, Chen Wei; Kuo, Chung Chih.

In: Brain Research, Vol. 1500, 15.03.2013, p. 28-35.

Research output: Contribution to journalArticle

Chiou, Ruei Jen ; Chang, Chen Wei ; Kuo, Chung Chih. / Involvement of the periaqueductal gray in the effect of motor cortexstimulation. In: Brain Research. 2013 ; Vol. 1500. pp. 28-35.
@article{0ba73826016642f79b202da2717dfb18,
title = "Involvement of the periaqueductal gray in the effect of motor cortexstimulation",
abstract = "Several clinical and animal studies of different pain models reported that motor cortex stimulation (MCS) has an antinociceptive effect. In our previous study, the response of the primary somatosensory cortex (SI) to peripheral stimuli decreased after MCS. The aim of the present study was to investigate involvement of the periaqueductal gray (PAG) in this inhibitory effect of MCS. Responses of the SI to electrical stimuli applied to both forepaws of anesthetized rats were monitored to evaluate the effect of MCS. After sensory-evoked potentials (SEPs) were stable, either saline, opioid, or dopamine receptor antagonists were locally microinjected into the PAG. After drug or saline administration, MCS was applied to the forepaw area of the right motor cortex. SEPs after MCS were compared to those before MCS. In the saline group, SEPs ipsilateral to MCS decreased, but SEPs contralateral to MCS did not. The decrease in SEPs was prevented by pretreatment of the PAG with naloxone. Application of a nonspecific dopamine receptor antagonist (α-flupenthixol) to the PAG also blocked the inhibition of SEPs after MCS. Inhibition of SEPs after MCS was blocked by local application of a D1 antagonist (SCH-23390) in the PAG, but not by a D2 antagonist (eticlopride). These results suggest that the PAG participates in the inhibitory effect of MCS, and this effect of MCS may be mediated by opioid and dopamine D1 receptors within thePAG.",
keywords = "Antinociception, Dopamine, Electrophysiology, Endogenous opioid, Pain modulation, Sensory-evoked potential",
author = "Chiou, {Ruei Jen} and Chang, {Chen Wei} and Kuo, {Chung Chih}",
year = "2013",
month = "3",
day = "15",
doi = "10.1016/j.brainres.2013.01.022",
language = "English",
volume = "1500",
pages = "28--35",
journal = "Brain Research",
issn = "0006-8993",
publisher = "Elsevier",

}

TY - JOUR

T1 - Involvement of the periaqueductal gray in the effect of motor cortexstimulation

AU - Chiou, Ruei Jen

AU - Chang, Chen Wei

AU - Kuo, Chung Chih

PY - 2013/3/15

Y1 - 2013/3/15

N2 - Several clinical and animal studies of different pain models reported that motor cortex stimulation (MCS) has an antinociceptive effect. In our previous study, the response of the primary somatosensory cortex (SI) to peripheral stimuli decreased after MCS. The aim of the present study was to investigate involvement of the periaqueductal gray (PAG) in this inhibitory effect of MCS. Responses of the SI to electrical stimuli applied to both forepaws of anesthetized rats were monitored to evaluate the effect of MCS. After sensory-evoked potentials (SEPs) were stable, either saline, opioid, or dopamine receptor antagonists were locally microinjected into the PAG. After drug or saline administration, MCS was applied to the forepaw area of the right motor cortex. SEPs after MCS were compared to those before MCS. In the saline group, SEPs ipsilateral to MCS decreased, but SEPs contralateral to MCS did not. The decrease in SEPs was prevented by pretreatment of the PAG with naloxone. Application of a nonspecific dopamine receptor antagonist (α-flupenthixol) to the PAG also blocked the inhibition of SEPs after MCS. Inhibition of SEPs after MCS was blocked by local application of a D1 antagonist (SCH-23390) in the PAG, but not by a D2 antagonist (eticlopride). These results suggest that the PAG participates in the inhibitory effect of MCS, and this effect of MCS may be mediated by opioid and dopamine D1 receptors within thePAG.

AB - Several clinical and animal studies of different pain models reported that motor cortex stimulation (MCS) has an antinociceptive effect. In our previous study, the response of the primary somatosensory cortex (SI) to peripheral stimuli decreased after MCS. The aim of the present study was to investigate involvement of the periaqueductal gray (PAG) in this inhibitory effect of MCS. Responses of the SI to electrical stimuli applied to both forepaws of anesthetized rats were monitored to evaluate the effect of MCS. After sensory-evoked potentials (SEPs) were stable, either saline, opioid, or dopamine receptor antagonists were locally microinjected into the PAG. After drug or saline administration, MCS was applied to the forepaw area of the right motor cortex. SEPs after MCS were compared to those before MCS. In the saline group, SEPs ipsilateral to MCS decreased, but SEPs contralateral to MCS did not. The decrease in SEPs was prevented by pretreatment of the PAG with naloxone. Application of a nonspecific dopamine receptor antagonist (α-flupenthixol) to the PAG also blocked the inhibition of SEPs after MCS. Inhibition of SEPs after MCS was blocked by local application of a D1 antagonist (SCH-23390) in the PAG, but not by a D2 antagonist (eticlopride). These results suggest that the PAG participates in the inhibitory effect of MCS, and this effect of MCS may be mediated by opioid and dopamine D1 receptors within thePAG.

KW - Antinociception

KW - Dopamine

KW - Electrophysiology

KW - Endogenous opioid

KW - Pain modulation

KW - Sensory-evoked potential

UR - http://www.scopus.com/inward/record.url?scp=84874646346&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=84874646346&partnerID=8YFLogxK

U2 - 10.1016/j.brainres.2013.01.022

DO - 10.1016/j.brainres.2013.01.022

M3 - Article

VL - 1500

SP - 28

EP - 35

JO - Brain Research

JF - Brain Research

SN - 0006-8993

ER -