Effect of excitatory and inhibitory agents and a glial inhibitor on optically-recorded primary-afferent excitation

Material type: 文書・図像類

Author: IKEDA, Hiroshiほか

Publisher: BioMed Central

Publication date: 2008-09-26

Material Format: Digital

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Note (General)：: The effects of GABA, excitatory amino-acid receptors antagonists and a glial metabolism inhibitor on primary-afferent excitation in the spinal dorsal ...

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Material Type: 文書・図像類
Title: Effect of excitatory and inhibitory agents and a glial inhibitor on optically-recorded primary-afferent excitation
Author/Editor: IKEDA, Hiroshi
KIRITOSHI, Takaki
MURASE, Kazuyuki
Author Heading: IKEDA, Hiroshi
KIRITOSHI, Takaki
MURASE, Kazuyuki
Publication, Distribution, etc.: BioMed Central
Publication Date: 2008-09-26
Publication Date (W3CDTF): 2008-09-26
Periodical title: Molecular Pain
No. or year of volume/issue: 4 39
Volume: 4
Issue: 39
ISSN (Periodical Title): ISSN : 1744-8069
Text Language Code: eng
Target Audience: 一般
Note (General): The effects of GABA, excitatory amino-acid receptors antagonists and a glial metabolism inhibitor on primary-afferent excitation in the spinal dorsal horn were studied by imaging the presynaptic excitation of high-threshold afferents in cord slices from young rats with a voltage-sensitive dye. Primary afferent fibers and terminals were anterogradely labeled with a voltage-sensitive dye from the dorsal root attached to the spinal cord slice. Single-pulse stimulation of C fiber-activating strength to the dorsal root elicited compound action potential-like optical responses in the superficial dorsal horn. The evoked presynaptic excitation was increased by the GABAA receptor antagonists picrotoxin and bicuculline, by glutamate receptor antagonists D-AP5 and CNQX, and by the glial metabolism inhibitor mono-fluoroacetic acid (MFA). The increase in presynaptic excitation by picrotoxin was inhibited in the presence of D-AP5, CNQX and MFA. Presynaptic modulation in the central terminal of fine primary afferents by excitatory and inhibitory amino acids may represent a mechanism that regulates the transmission of pain.
Access Restrictions: 限定公開
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