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- Nakagawa Takayuki
- Department of Molecular Pharmacology, Graduate School of Pharmaceutical Sciences, Kyoto University, Japan
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- Kaneko Shuji
- Department of Molecular Pharmacology, Graduate School of Pharmaceutical Sciences, Kyoto University, Japan
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抄録
Development of next-generation analgesics requires a better understanding of the molecular and cellular mechanisms underlying pathological pain. Accumulating evidence suggests that the activation of glia contributes to the central sensitization of pain signaling in the spinal cord. The role of microglia in pathological pain has been well documented, while that of astrocytes still remains unclear. After peripheral nerve inflammation or injury, spinal microglia are initially activated and subsequently sustained activation of astrocytes is precipitated, which are implicated in the induction and maintenance of pathological pain. Astrocytic activation is caused by the production of diffusible factors from primary afferent neurons (neuron-to-astrocyte signals) and activated microglia (microglia-to-astrocyte signals). Although astrocyte-to-neuron signals implicated in pathological pain is poorly understood, activated astrocytes, as well as microglia, produce proinflammatory cytokines and chemokines, which lead to adaptation of the dorsal horn neurons. Furthermore, it has been suggested that glial glutamate transporters in the spinal astrocytes are down-regulated in pathological pain and that up-regulation or functional enhancement of these transporters prevents pathological pain. This review will briefly discuss novel findings on the role of spinal astrocytes in pathological pain and their potential as a therapeutic target for novel analgesics.
収録刊行物
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- Journal of Pharmacological Sciences
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Journal of Pharmacological Sciences 114 (4), 347-353, 2010
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
- 1390282680157478016
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- NII論文ID
- 10029890649
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- NII書誌ID
- AA11806667
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- COI
- 1:CAS:528:DC%2BC3MXisFOnuw%3D%3D
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- ISSN
- 13478648
- 13478613
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- NDL書誌ID
- 10926397
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- PubMed
- 21081837
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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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- 抄録ライセンスフラグ
- 使用不可