Long-term potentiation of neuronal excitation by neuron-glia interactions in the rat spinal dorsal horn

Material type: 文書・図像類

Author: IKEDA, Hiroshiほか

Publisher: Blackwell

Publication date: 2007-03

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Note (General)：: By imaging neuronal excitation in rat spinal cord slices with a voltage-sensitive dye, we examined the role of glial cells in the P2X receptor agonist...

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Material Type: 文書・図像類
Title: Long-term potentiation of neuronal excitation by neuron-glia interactions in the rat spinal dorsal horn
Author/Editor: IKEDA, Hiroshi
TSUDA, Makoto
INOUE, Kazuhide
MURASE, Kazuyuki
Author Heading: IKEDA, Hiroshi
TSUDA, Makoto
INOUE, Kazuhide
MURASE, Kazuyuki
Publication, Distribution, etc.: Blackwell
Publication Date: 2007-03
Publication Date (W3CDTF): 2007-03
Periodical title: European Journal of Neuroscience
No. or year of volume/issue: 25 5
Volume: 25
Issue: 5
Pages: 1297-1306
ISSN (Periodical Title): ISSN : 0953-816X
Text Language Code: eng
Subject Heading: astrocyte
ATP
optical imaging
pain
Target Audience: 一般
Note (General): By imaging neuronal excitation in rat spinal cord slices with a voltage-sensitive dye, we examined the role of glial cells in the P2X receptor agonist αβ-methylene ATP (αβmeATP)-triggered long-term potentiation (LTP) in the dorsal horn. Bath application of αβmeATP potentiated neuronal excitation in the superficial dorsal horn. The potentiation was inhibited in the presence of the P2X receptor antagonists TNP-ATP, PPADS and A-317491, and was not induced in slices taken from rats neonatally treated with capsaicin. These results suggest that αβmeATP acts on P2X receptors, possibly P2X_3 and/or P2X_2/3, in capsaicin-sensitive primary afferent terminals. Furthermore, the potentiation was inhibited by treatment with the glial metabolism inhibitor monofluoroacetic acid. Results obtained with the p38 mitogen-activated protein kinase (p38 MAPK) inhibitor SB203580, tumour necrosis factor-α (TNF-α) and interleukin (IL)-6, and antibodies to TNF-α and IL-6, as well as by double immunolabelling of activated p38 MAPK with markers of astrocytes and microglia, demonstrated that αβmeATP activated p38 MAPK in astrocytes, and that the presence of proinflammatory cytokines and p38 MAPK activation were necessary for the induction of αβmeATP-triggered LTP. These findings indicate that glial cells contribute to the αβmeATP-induced LTP, which might be part of a cellular mechanism for the induction of persistent pain.
Access Restrictions: 限定公開
Rights (production): 〓 2007 Blackwell
Data Provider (Database): 国立情報学研究所 : 学術機関リポジトリデータベース（IRDB）（機関リポジトリ）
https://irdb.nii.ac.jp
Original Data Provider (Database): 福井大学 : 福井大学学術機関リポジトリ