• Koei Hayashi, Noriyuki Ozaki, Kenji Kawakita, Kazunori Itoh, Kazue Mizumura, Koichi Furukawa, Masaya Yasui, Kiyomi Hori, Shuang-Qin Yi, Takeshi Yamaguchi, and Yasuo Sugiura.
• Department of Functional Anatomy and Neuroscience, Nagoya University Graduate School of Medicine, Nagoya 466-8550, Japan.
• J Pain. 2011 Oct 1;12(10):1059-68.

UnlabelledMyofascial pain syndrome (MPS) is an important clinical condition characterized by chronic muscle pain and a myofascial trigger point (MTrP) located in a taut band (TB). However, its pathogenic mechanism is still unclear. We developed an animal model relevant to conditions of MPS, and analyzed the mechanism of the muscle pain in this model. We applied eccentric contraction (EC) to a rat's gastrocnemius muscle (GM) for 2 weeks, and examined the mechanical withdrawal thresholds, histological changes, and expressions and contents of nerve growth factor (NGF). The mechanical withdrawal threshold decreased significantly at the next day of first EC and continued up to 9 days after EC. TBs were palpable at 3 to 8 days after initiation of EC. In EC animals, necrotic and regenerating muscle cells were found significantly more than in control animals. In EC animals, NGF expressions in regenerating muscle cells and NGF contents of GM were significantly higher than control animals. Administration of NGF receptor (TrkA) inhibitor K252a showed significant suppression of mechanical hyperalgesia in EC animals. Repeated EC induced persistent mechanical muscle hyperalgesia associated with TB. NGF expressed in regenerating muscle cells may have an important role in persistent mechanical muscle hyperalgesia which might be relevant to pathogenesis of MPS.PerspectiveThe present study shows that NGF expressed in regenerating muscle cells is involved in persistent muscular mechanical hyperalgesia. NGF-TrkA signaling in primary muscle afferent neurons may be one of the most important and promising targets for MPS.Copyright © 2011 American Pain Society. Published by Elsevier Inc. All rights reserved.

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