Activation of Different Signals Identified with Glia Cells Contribute to the Progression of HyperalgesiaReportar como inadecuado

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Cellular and Molecular Neurobiology

, Volume 33, Issue 2, pp 167–174

First Online: 23 October 2012Received: 04 August 2012Accepted: 04 October 2012


Hyperalgesia results from a decreased pain threshold, often subsequent to peripheral tissue damage. Recent reports revealed several promising mechanisms of hyperalgesia, but many issues remain unclear. The glial activation accompanying inflammation of neurotransmission in the spinal cord might be related to the initiation and maintenance of hyperalgesia. The present study investigated the pharmacological pain-modifying effects of mitogen-associated protein kinase MAPK-related inhibitors identified with glia cells over time during inflammatory pain. A model of inflammatory pain was produced by injecting mustard oil MO into the hind paws of rats. Following MO injection, the changes in paws flinching as the early onset of pain and paw withdrawal latency PWL in response to thermal stimulation were measured as delayed-onset hyperalgesia. Before and after the MO injection, one of the inhibitors, a p38-MAPK SB, nuclear factor NF-κB PDTC, BDNF-trk-B K252a, or JNK-1 SP, was administered and flinching and PWL were measured. In the SB, PDTC, and k252a groups, early flinching following MO injection was moderately suppressed. Hyperalgesia was significantly suppressed in the left–right difference of PWL in animals receiving SB, k252a, or PDTC pre-treatment. In animals receiving post-treatment, the suppressive effects were most potent in the SP group. The present results revealed that microglial activation resulting from the release of the phosphatase p38-MAPK, the transcription factor NF-κB, and BDNF contributes to the early stage of inflammatory pain. Astrocyte activation accompanying JNK activation contributes to subsequent hyperalgesia. Activation of different signals identified with glia cells is thought to contribute to the progression of hyperalgesia, which represents an applicable finding for the treatment of hyperalgesia.

KeywordsBDNF Hyperalgesia JNK Neuroglia interaction p38-MAPK  Download fulltext PDF

Autor: Satoru Yamamoto - Yusuke Kishishita - Mitsuhiro Yoshida - Daisuke Miura - Hidenori Suzuki - Kozo Ishikawa - Hirofumi Miyaza


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