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Updated: Aug 16, 2026

Patch Clamp Recordings on Intact Dorsal Root Ganglia from Adult Rats
Published on: September 29, 2016
c-Jun N-terminal kinase activation in dorsal root ganglion contributes to pain hypersensitivity
Hideo Doya1, Seiji Ohtori, Masashi Fujitani
1Department of Neurobiology, Graduate School of Medicine, Chiba University, 1-8-1 Inohana, Chuo-ku, Chiba 260-8670, Japan.
Abstract:
Inflammatory pain, characterized by a decrease in the nociceptive threshold, arises through the actions of inflammatory mediators. Mitogen-activated protein kinase cascades participate in peripheral nociceptive sensitization. We examined the involvement of c-Jun N-terminal kinase (JNK) in the dorsal root ganglion (DRG) in the early phase of inflammation-induced hyperalgesia. An intra-plantar (i.pl.) injection of complete Freund's adjuvant induced the activation of JNK in DRG neurons within 30 min. Pre-treatment as well as post-treatment of rats with a JNK inhibitor, SP600125, significantly attenuated thermal hyperalgesia, as assessed by paw-withdrawal latency, and the upregulation of c-fos immunoreactivity in dorsal horn neurons. An i.pl. injection of nerve growth factor (NGF) also induced the phosphorylation of JNK as well as thermal hyperalgesia, and SP600125 improved hyperalgesia. Inhibitor experiments suggest that JNK and extracellular signal-regulated protein kinase act on primary nociceptive neurons synergistically. These findings demonstrate that JNK is a therapeutic target for treating inflammation-induced pain hypersensitivity.
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