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Activation of extracellular signal‐regulated protein kinases 5 in primary afferent neurons contributes to heat and cold hyperalgesia after inflammation
Author(s) -
Katsura Hirokazu,
Obata Koichi,
Mizushima Toshiyuki,
Sakurai Jun,
Kobayashi Kimiko,
Yamanaka Hiroki,
Dai Yi,
Fukuoka Tetsuo,
Sakagami Masafumi,
Noguchi Koichi
Publication year - 2007
Publication title -
journal of neurochemistry
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.75
H-Index - 229
eISSN - 1471-4159
pISSN - 0022-3042
DOI - 10.1111/j.1471-4159.2007.04698.x
Subject(s) - inflammation , dorsal root ganglion , hyperalgesia , trpv1 , trpm8 , phosphorylation , extracellular , microbiology and biotechnology , kinase , signal transduction , sensory neuron , transient receptor potential channel , chemistry , medicine , neuroscience , receptor , biology , sensory system , nociception
Heat and cold hyperalgesia is a common feature of inflammatory pain. To investigate whether activation of extracellular signal‐regulated protein kinase 5 (ERK5), also known as big mitogen‐activated protein kinase 1, in primary sensory neurons participates in inflammatory pain, we examined the phosphorylation of ERK5 in the dorsal root ganglion (DRG) after peripheral inflammation. Inflammation induced by complete Freund’s adjuvant produced heat and cold hyperalgesia on the ipsilateral hind paw and induced an increase in the phosphorylation of ERK5, mainly in tyrosine kinase A‐expressing small‐ and medium‐size neurons. In contrast, there was no change in ERK5 phosphorylation in the spinal dorsal horn. ERK5 antisense, but not mismatch, oligodeoxynucleotide decreased the activation of ERK5 and suppressed inflammation‐induced heat and cold hyperalgesia. Furthermore, the inhibition of ERK5 blocked the induction of transient receptor potential channel TRPV1 and TRPA1 expression in DRG neurons after peripheral inflammation. Our results show that ERK5 activated in DRG neurons contribute to the development of inflammatory pain. Thus, blocking ERK5 signaling in sensory neurons that has the potential for preventing pain after inflammation.