ID 103613
著者
樋浦, 明夫 Oral Histology, School of Dentistry, University of Tokushima KAKEN研究者をさがす
中川, 弘 Dentistry for Persons with Disability, Tokushima niversity Hospital, University of Tokushima 徳島大学 教育研究者総覧 KAKEN研究者をさがす
キーワード
Glias
TRP channels
Inflammatory soup
Abnormal pain
Acute noxious heat pain
資料タイプ
学術雑誌論文
抄録
Nowadays, one cannot but recognize a key role of the peripheral and central glial cells for generation of clinical neuropathic pain. Many cytokines are released from glial cells, immune cells and nociceptive primary afferent central or peripheral terminals by injury, bacterial or viral infection, and envenomation by bee venom or scorpion. Released cytokines mutually affect by paracrine or autocrine manner among glias, immune cells and neurons, thereby produce and transmit the exaggerating pain information to the brain. Indeed, suppression of activated glia and immune cells by chemical agents or antibodies can relief abnormal pain caused by various experimental neuropathies. Thus, abnormal exaggerated pain cannot be explained without the role of glia and immune cells. Many investigators emphasized that therapeutic use of inactivating agents to glial and immune cells but not to neurons is available for alleviation of clinical pain. Thermo-TRP channels, TRPV1, TRPA1 and TRPM8 could not sense neuropathic pain by themselves without close interactions between glias, immune cells and TRP channels. The removal of persistent clinical pain will be rescued by treatment with inactivating chemicals to glias and immune cells. In addition, physiological noxious heat could be sensed by unknown sensor other than thermo-TRP channels, TRPV1, TRPA1 and TRPM8
掲載誌名
WebmedCentral PAIN
ISSN
20461690
出版者
WebmedCentral
3
9
開始ページ
WMC003728
発行日
2012-09-27
備考
Article URL: http://www.webmedcentral.com/article_view/3728

This is an open-access article distributed under the terms of the Creative Commons Attribution
License(CC-BY), which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.
EDB ID
257215
出版社版DOI
出版社版URL
フルテキストファイル
言語
eng
著者版フラグ
出版社版
部局
病院
歯学系