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Pain matrix shift in the rat brain following persistent colonic inflammation revealed by voxel-based statistical analysis.
https://repo.qst.go.jp/records/78035
https://repo.qst.go.jp/records/78035af69961f-f483-43ba-b89f-8fc7a26a626f
Item type | 学術雑誌論文 / Journal Article(1) | |||||
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公開日 | 2019-12-17 | |||||
タイトル | ||||||
タイトル | Pain matrix shift in the rat brain following persistent colonic inflammation revealed by voxel-based statistical analysis. | |||||
言語 | ||||||
言語 | eng | |||||
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資源タイプ識別子 | http://purl.org/coar/resource_type/c_6501 | |||||
資源タイプ | journal article | |||||
アクセス権 | ||||||
アクセス権 | metadata only access | |||||
アクセス権URI | http://purl.org/coar/access_right/c_14cb | |||||
著者 |
Huang, Tianliang
× Huang, Tianliang× Okauchi, Takashi× Hu, Di× Shigeta, Mika× Wu, Yuping× Wada, Yasuhiro× Hayashinaka, Emi× Wang, Shenglan× Kogure, Yoko× Noguchi, Koichi× Watanabe, Yasuyoshi× Dai, Yi× Cui, Yilong× Takashi, Okauchi |
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抄録 | ||||||
内容記述タイプ | Abstract | |||||
内容記述 | Inflammatory bowel disease (IBD), mainly comprising Crohn’s disease and ulcerative colitis, is characterized by chronic inflammation in the digestive tract. Approximately 60% of the patients experience abdominal pain during acute IBD episodes, which severely impairs their quality of life. Both peripheral and central mechanisms are thought to be involved in such abdominal pain in IBD. Although much attention has been paid to peripheral mechanisms of abdominal pain in IBD pathophysiology, the involvement of supraspinal mechanisms remains poorly understood. To address this issue, we investigated regional brain activity in response to colorectal distension (CRD) in normal and IBD model rats using voxel-based statistical analysis of 2-deoxy-2-[18F]fluoro-D-glucose (FDG) PET imaging. The rat IBD model was generated by colorectal administration of 2,4,6-trinitrobenzene sulfonic acid (TNBS), a chemical compound widely used to generate colitis. Tissue damage and inflammation were induced and dynamically changed with time after TNBS injection, while CRD-induced visceromotor response showed corresponding temporal changes. We found that characteristic brain activations were observed in response to visceral innocuous and noxious CRD and supraspinal nociception shared some physiological sensory pathway. Moreover, widespread brain regions were activated, and the functional coupling between the central medial thalamic nucleus (CMT) and anterior cingulate cortex (ACC) was enhanced after noxious CRD in IBD model of rats. Increased brain activity in the anterior insular cortex (aINS) and ACC positively correlated with noxious CRD-induced pain severity in normal and IBD rats respectively. These findings suggest that the pain matrix was shifted following persistent colonic inflammation, and thalamocortical sensitization in the pathway from CMT to ACC might be a central mechanism of the visceral hyperalgesia in IBD pathophysiology. | |||||
書誌情報 |
Molecular pain 巻 15, p. 1744806919891327, 発行日 2019-11 |
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出版者 | ||||||
出版者 | Sage Publications Inc. | |||||
ISSN | ||||||
収録物識別子タイプ | ISSN | |||||
収録物識別子 | 1744-8069 | |||||
PubMed番号 | ||||||
識別子タイプ | PMID | |||||
関連識別子 | 31709891 | |||||
DOI | ||||||
識別子タイプ | DOI | |||||
関連識別子 | 10.1177/1744806919891327 | |||||
関連サイト | ||||||
識別子タイプ | URI | |||||
関連識別子 | https://journals.sagepub.com/doi/pdf/10.1177/1744806919891327 |