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日本学術振興会先端研究拠点事業共催:痛み研究最前線
JSPS Core-to-Core Program:The front line of pain research

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開催日
2010年09月04日(土)
時 間
08:30 - 11:00
会 場
Room 1
Chairperson(s)
柿木 隆介 / Ryusuke Kakigi (自然科学研究機構 生理学研究所 統合生理研究系 / Department of Integrative Physiology, National Institute for Physiological Sciences)
水村 和枝 / Kazue Mizumura (名古屋大学環境医学研究所 神経系分野II / Dept. Neurosci. II, Res. Inst. Environ. Med., Nagoya Univ., Nagoya 464-8601, Japan)

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筋性疼痛における神経成長因子(NGF)の役割
Role of nerve growth factor (NGF) in muscular pain

演題番号 : S3-1-1-3

水村 和枝 / Kazue Mizumura:1 村瀬 詩織 / Shiori Murase:1 田口 徹 / Toru Taguchi:1 鈴木 実佳子 / Mikako Suzuki:1,2 

1:名古屋大学環境医学研究所 神経系分野II / Dept. Neurosci. II, Res. Inst. Environ. Med., Nagoya Univ., Nagoya 464-8601, Japan 2:名古屋大学大学院医学系研究科手の外科学分野 / Dept. Hand Surg., Grad. Sch.Med., Nagoya Univ., Nagoya 466-8550, Japan 

 

Overall prevalence of musculoskeletal pain is very high and it treatment and prevention are urgent issues for our aging society. However, its neural mechanism is largely unknown. Recently, particular attention has been focused on NGF in the muscle pain research since it had been reported that intramuscular injection (i.m.) of NGF in human subjects elicited strong and long-lasting mechanical hyperalgesia without pain at rest. However, muscular conditions in which NGF is involved have not been known except inflammation. We found NGF plays a pivotal role in muscle mechanical hyperalgesia (delayed onset muscle soreness, DOMS) after lengthening contraction (LC) without any clear signs of inflammation: NGF was upregulated in the muscle 12 hours - 2 days after LC, and i.m. of antibodies to NGF 2 days after LC reversed the muscle mechanical hyperalgesia (Murase et al., 2010). Muscle thin fiber receptors recorded in vitro were sensitized to mechanical stimulation 2 days after LC at the peak of DOMS (Taguchi et el., 2005) and NGF is responsible for this sensitization. This means NGF-induced sensitization of muscle nociceptors is mostly a peripheral event. In addition, we found that bradykinin released during LC plays a pivotal role in triggering the process that leads to NGF upregulation and DOMS but not in maintaining DOMS by directly sensitizing nociceptors. Thus, NGF upregulation through activation of B2 bradykinin receptors is essential for DOMS. DOMS has similarities with clinically important pain conditions such as myofascial pain syndrome and is often used as a model for its study. NGF upregulation was also found in the muscle in a neuropathic pain model (spinal nerve ligation/cut at L5), and its muscular mechanical hyperalgesia was reversed by i.m. of anti-NGF antibody. These results suggest that muscles are algesic substance (such as NGF) producing organ, and that, besides nociceptive pathways, muscle itself must be studied for understanding muscle pain.

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