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Spinal NMDA-receptor dependent amplification of nociceptive transmission to rat primary somatosensory cortex (SI).

Kalliomäki, Jarkko; Granmo, Marcus LU and Schouenborg, Jens LU (2003) In Pain 104(1-2). p.195-200
Abstract
The role of NMDA mechanisms in spinal pathways mediating acute nociceptive input to the somatosensory cortex is not clear. In this study, the effect of NMDA-antagonists on nociceptive C fibre transmission to the primary somatosensory cortex (SI) was investigated. Cortical field potentials evoked by CO2-laser stimulation of the skin were recorded in the halothane/nitrous oxide anaesthetized rat.



The SI nociceptive evoked potential (EP) amplitudes were dependent on the frequency of noxious heat stimulation. The amplitudes of SI potentials evoked by CO2-laser pulses (duration 15–20 ms, stimulation energy 21–28 mJ/mm2) delivered at a frequency of 0.1 Hz were approximately 40% of the amplitudes of potentials evoked by 1.0 Hz... (More)
The role of NMDA mechanisms in spinal pathways mediating acute nociceptive input to the somatosensory cortex is not clear. In this study, the effect of NMDA-antagonists on nociceptive C fibre transmission to the primary somatosensory cortex (SI) was investigated. Cortical field potentials evoked by CO2-laser stimulation of the skin were recorded in the halothane/nitrous oxide anaesthetized rat.



The SI nociceptive evoked potential (EP) amplitudes were dependent on the frequency of noxious heat stimulation. The amplitudes of SI potentials evoked by CO2-laser pulses (duration 15–20 ms, stimulation energy 21–28 mJ/mm2) delivered at a frequency of 0.1 Hz were approximately 40% of the amplitudes of potentials evoked by 1.0 Hz stimulation.



After intrathecal lumbar application of either of the NMDA-antagonists CPP or MK-801, the amplitudes of nociceptive SI potentials, evoked by 1.0 Hz stimulation of the contralateral hindpaw, were reduced to approximately 40% of controls. By contrast, field potentials evoked by 0.1 Hz stimulation of the hindpaw were unaffected by MK-801.



SI potentials evoked by 1.0 Hz stimulation of the contralateral forepaw did not change after lumbar application of CPP or MK-801, indicating that the depression of hindpaw EPs was due to a segmental effect in the spinal cord.



It is concluded that spinal NMDA-receptor mechanisms amplify the acute transmission of nociceptive C fiber input to SI in a frequency-dependent way. (Less)
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author
organization
publishing date
type
Contribution to journal
publication status
published
subject
keywords
C fibre, Nociception, Pain, Somatosensory cortex, NMDA-receptor, Wind-up
in
Pain
volume
104
issue
1-2
pages
195 - 200
publisher
Elsevier
external identifiers
  • wos:000184262700021
  • pmid:12855329
  • scopus:0037823487
ISSN
1872-6623
DOI
language
English
LU publication?
yes
id
20f4d8e8-b8f6-4f1f-af9b-968f4a449493 (old id 116665)
alternative location
http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=12855329&dopt=Abstract
date added to LUP
2007-07-16 11:31:46
date last changed
2018-05-29 11:00:14
@article{20f4d8e8-b8f6-4f1f-af9b-968f4a449493,
  abstract     = {The role of NMDA mechanisms in spinal pathways mediating acute nociceptive input to the somatosensory cortex is not clear. In this study, the effect of NMDA-antagonists on nociceptive C fibre transmission to the primary somatosensory cortex (SI) was investigated. Cortical field potentials evoked by CO2-laser stimulation of the skin were recorded in the halothane/nitrous oxide anaesthetized rat.<br/><br>
<br/><br>
The SI nociceptive evoked potential (EP) amplitudes were dependent on the frequency of noxious heat stimulation. The amplitudes of SI potentials evoked by CO2-laser pulses (duration 15–20 ms, stimulation energy 21–28 mJ/mm2) delivered at a frequency of 0.1 Hz were approximately 40% of the amplitudes of potentials evoked by 1.0 Hz stimulation.<br/><br>
<br/><br>
After intrathecal lumbar application of either of the NMDA-antagonists CPP or MK-801, the amplitudes of nociceptive SI potentials, evoked by 1.0 Hz stimulation of the contralateral hindpaw, were reduced to approximately 40% of controls. By contrast, field potentials evoked by 0.1 Hz stimulation of the hindpaw were unaffected by MK-801.<br/><br>
<br/><br>
SI potentials evoked by 1.0 Hz stimulation of the contralateral forepaw did not change after lumbar application of CPP or MK-801, indicating that the depression of hindpaw EPs was due to a segmental effect in the spinal cord.<br/><br>
<br/><br>
It is concluded that spinal NMDA-receptor mechanisms amplify the acute transmission of nociceptive C fiber input to SI in a frequency-dependent way.},
  author       = {Kalliomäki, Jarkko and Granmo, Marcus and Schouenborg, Jens},
  issn         = {1872-6623},
  keyword      = {C fibre,Nociception,Pain,Somatosensory cortex,NMDA-receptor,Wind-up},
  language     = {eng},
  number       = {1-2},
  pages        = {195--200},
  publisher    = {Elsevier},
  series       = {Pain},
  title        = {Spinal NMDA-receptor dependent amplification of nociceptive transmission to rat primary somatosensory cortex (SI).},
  url          = {http://dx.doi.org/},
  volume       = {104},
  year         = {2003},
}