Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
3
pubmed:dateCreated
2005-5-24
pubmed:abstractText
Postoperative pain significantly impacts patient recovery. However, postoperative pain management remains suboptimal, perhaps because treatment strategies are based mainly on studies using inflammatory pain models. We used a recently developed mouse model of incisional pain to investigate peripheral and spinal mechanisms contributing to heat hyperalgesia after incision. Behavioral experiments involving TRPV1 KO mice demonstrate that, as previously observed in inflammatory models, TRPV1 is necessary for heat (but not mechanical) hyperalgesia after incision. However, in WT mice, neither the proportion of TRPV1 immunoreactive neurons in the DRG nor the intensity of TRPV1 staining in the sciatic nerve was different from that in controls up to 4 days after incision. This result was corroborated by immunoblot analysis of sciatic nerve in rats subjected to an incision, and is distinct from that following inflammation of the rat hind paw, a situation in which TRPV1 expression levels in sciatic nerve increases. In the absence of heat exposure, spinal c-Fos staining was similar between incised TRPV1 KO and WT mice. However, differences in c-Fos staining between heat exposed TRPV1 KO and WT mice after incision suggest that the incision-mediated enhancement of heat-evoked signaling to the spinal cord involves a TRPV1-dependent mechanism. Finally, heat hyperalgesia after incision was reversed by antagonism of spinal non-NMDA receptors, unlike inflammatory hyperalgesia, which is mediated via NMDA receptors . Thus, TRPV1 is important for the generation of thermal hyperalgesia after incision. Our observations suggest that all experimental pain models may not be equally appropriate to guide the development of postoperative pain therapies.
pubmed:grant
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Jun
pubmed:issn
0304-3959
pubmed:author
pubmed:issnType
Print
pubmed:volume
115
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
296-307
pubmed:dateRevised
2008-11-21
pubmed:meshHeading
pubmed-meshheading:15911156-Animals, pubmed-meshheading:15911156-Dizocilpine Maleate, pubmed-meshheading:15911156-Excitatory Amino Acid Antagonists, pubmed-meshheading:15911156-Female, pubmed-meshheading:15911156-Hot Temperature, pubmed-meshheading:15911156-Hyperalgesia, pubmed-meshheading:15911156-Ion Channels, pubmed-meshheading:15911156-Male, pubmed-meshheading:15911156-Mice, pubmed-meshheading:15911156-Mice, Inbred C57BL, pubmed-meshheading:15911156-Mice, Knockout, pubmed-meshheading:15911156-Neurogenic Inflammation, pubmed-meshheading:15911156-Nociceptors, pubmed-meshheading:15911156-Pain, Postoperative, pubmed-meshheading:15911156-Physical Stimulation, pubmed-meshheading:15911156-Proto-Oncogene Proteins c-fos, pubmed-meshheading:15911156-Quinoxalines, pubmed-meshheading:15911156-Skin, pubmed-meshheading:15911156-TRPV Cation Channels
pubmed:year
2005
pubmed:articleTitle
Heat hyperalgesia after incision requires TRPV1 and is distinct from pure inflammatory pain.
pubmed:affiliation
Department of Anesthesiology, Johns Hopkins University, Baltimore, MD, USA. pogatzki@anit.uni-muenster.de
pubmed:publicationType
Journal Article, Research Support, U.S. Gov't, P.H.S., Research Support, Non-U.S. Gov't, Research Support, N.I.H., Extramural