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Severe burn injury induces a characteristic activation of extracellular signal‐regulated kinase 1/2 in spinal dorsal horn neurons
Author(s) -
Whitel John P.M.,
Kol Chin Wing,
Fidalgol Antonio Rei,
Cibellil Mario,
Paulel Cleoper C.,
Andersonl Peter J.,
Cruzl Celia,
Gombal Szabolcs,
Mateszl Klara,
Veressl Gabor,
Avelinol Antonio,
Nagyl Istvan
Publication year - 2011
Publication title -
european journal of pain
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.305
H-Index - 109
eISSN - 1532-2149
pISSN - 1090-3801
DOI - 10.1016/j.ejpain.2010.12.006
Subject(s) - scalding , trpv1 , nociception , neuropathic pain , extracellular , spinal cord , french horn , dorsum , noxious stimulus , medicine , peripheral nerve injury , nociceptor , nerve injury , neuroscience , chemistry , anatomy , anesthesia , receptor , biology , transient receptor potential channel , sciatic nerve , biochemistry , psychology , pedagogy , food science
We have studied scalding‐type burn injury‐induced activation of extracellular signal‐regulated kinase 1/2 (ERK1/2) in the spinal dorsal horn, which is a recognised marker for spinal nociceptive processing. At 5 min after severe scalding injury to mouse hind‐paw, a substantial number of phosphorylated ERK1/2 (pERK1/2) immunopositive neurons were found in the ipsilateral dorsal horn. At 1 h post‐injury, the number of pERK1/2‐labelled neurons remained substantially the same. However, at 3 h post‐injury, a further increase in the number of labelled neurons was found on the ipsilateral side, while a remarkable increase in the number of labelled neurons on the contralateral side resulted in there being no significant difference between the extent of the labelling on both sides. By 6 h post‐injury, the number of labelled neurons was reduced on both sides without there being significant difference between the two sides. A similar pattern of severe scalding injury‐induced activation of ERK1/2 in spinal dorsal horn neurons over the same time‐course was found in mice which lacked the transient receptor potential type 1 receptor (TRPV1) except that the extent to which ERK1/2 was activated in the ipsilateral dorsal horn at 5 min post‐injury was significantly greater in wild‐type animals when compared to TRPV1 null animals. This difference in activation of ERK1/2 in spinal dorsal horn neurons was abolished within 1 h after injury, demonstrating that TRPV1 is not essential for the maintenance of ongoing spinal nociceptive processing in inflammatory pain conditions in mouse resulting from at least certain types of severe burn injury.