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Symposia

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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神経障害性疼痛とミクログリア活性化
Microglia activation in neuropathic pain

演題番号 : S3-1-1-5

井上 和秀 / Kazuhide Inoue:1 津田 誠 / Makoto Tsuda:1 

1:九州大学 薬学研究院 / Faculty of Pharmaceutical Sciences, Kyushu University 

 

Neuropathic pain is a highly debilitating chronic pain that occurs after nerve injury and is resistant to currently available treatments. We have shown that activating P2X4R upregulated in spinal microglia after nerve injury contributes to neuropathic pain (Nature, 2003), and the stimulation of P2X4Rs causes release of brain-derived neurotrophic factor (BDNF) evoking a collapse of their transmembrane anion gradient and the subsequent neuronal hyper-excitability (Nature, 2005). These receptors are expressed in activated microglia in response to peripheral nerve injury, but the mechanisms underlying activation of microglia following nerve injury remains to be determined. We recently found that a single intrathecal administration of IFN-&gamma to normal animals produces a long-lasting tactile allodynic behavior and activation of microglia in the spinal cord. The expression of IFN-&gamma receptor mRNA in the spinal cord is localized predominantly in microglia (PNAS 2009). IFN-&gamma evoked P2X4 up-regulation in microglia. Furthermore, IFN-&gamma receptor-deficient mice (ifngr-/-) exhibited a striking reduction in nerve injury-induced tactile allodynia and in the increase in microglial cells with hypertrophic morphology. These findings suggest that IFN-&gamma signaling through IFN-&gammaR plays as a crucial trigger of microglia activation after nerve injury and the subsequent tactile allodynia.

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