Current Perspective : Microglial Regulation of Neuropathic Pain
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- Tsuda Makoto
- Department of Molecular and System Pharmacology, Graduate School of Pharmaceutical Sciences, Kyushu University, Japan
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- Masuda Takahiro
- Department of Molecular and System Pharmacology, Graduate School of Pharmaceutical Sciences, Kyushu University, Japan
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- Tozaki-Saitoh Hidetoshi
- Department of Molecular and System Pharmacology, Graduate School of Pharmaceutical Sciences, Kyushu University, Japan
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- Inoue Kazuhide
- Department of Molecular and System Pharmacology, Graduate School of Pharmaceutical Sciences, Kyushu University, Japan
書誌事項
- タイトル別名
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- Microglial Regulation of Neuropathic Pain
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Neuropathic pain is a highly debilitating chronic pain state that is a consequence of nerve injury or of diseases such as diabetes, cancer, infection, autoimmune disease, or trauma. Neuropathic pain is often resistant to currently available analgesics. There is a rapidly growing body of evidence indicating that signalings from spinal microglia play crucial roles in the pathogenesis of neuropathic pain. After peripheral nerve injury, microglia transform to reactive states through the expression of various genes such as cell-surface receptors (including purinergic receptors) and proinflammatory cytokines that enhance synaptic transmission in dorsal horn neurons. Inhibiting function or expression of these microglial molecules strongly suppresses pain hypersensitivity to innocuous mechanical stimuli (tactile allodynia), a hallmark symptom of neuropathic pain. A recent study also reveals that the transcription factor IRF8 (interferon regulatory factor 8) is a critical regulator of the nerve injury–induced gene expression in microglia. The present review article highlights the recent advances in our understanding of spinal microglia in neuropathic pain.
収録刊行物
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- Journal of Pharmacological Sciences
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Journal of Pharmacological Sciences 121 (2), 89-94, 2013
公益社団法人 日本薬理学会
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詳細情報 詳細情報について
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- CRID
- 1390001205180999040
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- NII論文ID
- 10031156937
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- NII書誌ID
- AA11806667
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- COI
- 1:CAS:528:DC%2BC3sXjvVyju70%3D
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- ISSN
- 13478648
- 13478613
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- NDL書誌ID
- 024274877
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- PubMed
- 23337437
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- 本文言語コード
- en
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- データソース種別
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- JaLC
- NDL
- Crossref
- PubMed
- CiNii Articles
- KAKEN
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