To the descending pain-control system in rats, inflammation-induced primary and secondary hyperalgesia are two different things
- PMID: 15135934
- DOI: 10.1016/j.neulet.2003.12.002
To the descending pain-control system in rats, inflammation-induced primary and secondary hyperalgesia are two different things
Abstract
The periaqueductal gray matter and the rostral ventromedial medulla (RVM), with its projections to the spinal dorsal horn, constitute the efferent channel of the 'descending pain-control system'. Noxious stimulation of a peripheral tissue causes more pain if this tissue is inflamed (primary hyperalgesia). In such cases, stimulation of neighboring but uninflamed tissues also becomes more painful (secondary hyperalgesia). In animal models of inflammation, the descending pain-control system sends down, simultaneously, inhibitory and facilitatory influences, but inhibition predominates for primary hyperalgesia while facilitation predominates for secondary hyperalgesia. Descending inhibition and facilitation during peripheral inflammation are due not only to previously existing descending modulation, but also to inflammation-induced changes in RVM which involve receptors for NMDA, AMPA, cholecystokinin and neurotensin, as well as synthesis of enkephalins and nitric oxide.
Similar articles
-
Descending control of persistent pain: inhibitory or facilitatory?Brain Res Brain Res Rev. 2004 Nov;46(3):295-309. doi: 10.1016/j.brainresrev.2004.07.004. Brain Res Brain Res Rev. 2004. PMID: 15571771 Review.
-
Differential mediation of descending pain facilitation and inhibition by spinal 5HT-3 and 5HT-7 receptors.Brain Res. 2009 Jul 14;1280:52-9. doi: 10.1016/j.brainres.2009.05.001. Epub 2009 May 8. Brain Res. 2009. PMID: 19427839
-
Prostaglandin E2 in the midbrain periaqueductal gray produces hyperalgesia and activates pain-modulating circuitry in the rostral ventromedial medulla.Pain. 2004 Jul;110(1-2):419-26. doi: 10.1016/j.pain.2004.04.026. Pain. 2004. PMID: 15275794
-
Trigeminal transition zone/rostral ventromedial medulla connections and facilitation of orofacial hyperalgesia after masseter inflammation in rats.J Comp Neurol. 2005 Dec 26;493(4):510-23. doi: 10.1002/cne.20797. J Comp Neurol. 2005. PMID: 16304628
-
Descending modulation of pain.Neurosci Biobehav Rev. 2004 Jan;27(8):729-37. doi: 10.1016/j.neubiorev.2003.11.008. Neurosci Biobehav Rev. 2004. PMID: 15019423 Review.
Cited by
-
Inhibition of NLRP3 Inflammasome Prevents LPS-Induced Inflammatory Hyperalgesia in Mice: Contribution of NF-κB, Caspase-1/11, ASC, NOX, and NOS Isoforms.Inflammation. 2017 Apr;40(2):366-386. doi: 10.1007/s10753-016-0483-3. Inflammation. 2017. PMID: 27924425
-
The role of neurotensin in central nervous system pathophysiology: what is the evidence?J Psychiatry Neurosci. 2006 Jul;31(4):229-45. J Psychiatry Neurosci. 2006. PMID: 16862241 Free PMC article. Review.
-
Roles of reactive oxygen and nitrogen species in pain.Free Radic Biol Med. 2011 Sep 1;51(5):951-66. doi: 10.1016/j.freeradbiomed.2011.01.026. Epub 2011 Jan 28. Free Radic Biol Med. 2011. PMID: 21277369 Free PMC article. Review.
-
Distribution of glycine/GABA neurons in the ventromedial medulla with descending spinal projections and evidence for an ascending glycine/GABA projection.PLoS One. 2012;7(4):e35293. doi: 10.1371/journal.pone.0035293. Epub 2012 Apr 30. PLoS One. 2012. PMID: 22558137 Free PMC article.
-
Periaqueductal Grey EP3 Receptors Facilitate Spinal Nociception in Arthritic Secondary Hypersensitivity.J Neurosci. 2016 Aug 31;36(35):9026-40. doi: 10.1523/JNEUROSCI.4393-15.2016. J Neurosci. 2016. PMID: 27581447 Free PMC article.
Publication types
MeSH terms
Substances
LinkOut - more resources
Full Text Sources
Medical