To elucidate the mechanism of pain induced inhibitory neural circuit plasticity in amygdala
| Project/Area Number |
15K08665
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| Research Category |
Grant-in-Aid for Scientific Research (C)
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| Allocation Type | Multi-year Fund |
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| Section | 一般 |
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| Research Field |
Pain science
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| Research Institution | University of Tsukuba |
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Principal Investigator |
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| Project Period (FY) |
2015-04-01 – 2019-03-31
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| Project Status |
Completed (Fiscal Year 2018)
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| Budget Amount *help |
¥4,810,000 (Direct Cost: ¥3,700,000、Indirect Cost: ¥1,110,000)
Fiscal Year 2017: ¥1,560,000 (Direct Cost: ¥1,200,000、Indirect Cost: ¥360,000)
Fiscal Year 2016: ¥1,950,000 (Direct Cost: ¥1,500,000、Indirect Cost: ¥450,000)
Fiscal Year 2015: ¥1,300,000 (Direct Cost: ¥1,000,000、Indirect Cost: ¥300,000)
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| Keywords | 扁桃体 / プレガバリン / 疼痛 / 侵害受容 / 炎症性疼痛モデル / 扁桃体中心核 / 神経炎症性疼痛 / 外側腕傍核 / 扁桃体基底外側部 / Pregabalin / 炎症性疼痛 / 扁桃体外側基底核 / 痛み / ホルマリン |
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| Outline of Final Research Achievements |
Pregabalin (PGB) is used for the peripheral and central neuropathic pain. Its mechanisms are selective binding to the α2δ subunit of voltage-gated calcium channels and reduce excitatory eurotransmitter release. The central nucleus amygdala (CeA) is a kernel site for the enhanced nociception-emotion link in the chronic pain. The nociceptive information is conveyed to CeA via two pathways. One is thalamocortical pathway that the projections from the basolateral amygdala (BLA) and the other is spinoparabrachial pathway that convey nociceptive informations directly from the externalpart of the pontine lateral parabrachial nucleus (LPB). We compared the effects of PGB on these excitatory inputs using formalin-treated inflammatory pain model mice. PGB inhibits the BLA to CeA transmission, but not the LPB to CeA, through a mechanism involving reduced release probability, particularly in inflammation conditions. These rsults suggests that PGB in treating the cognito-affective aspect of pain.
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| Academic Significance and Societal Importance of the Research Achievements |
本邦の慢性疼痛患者は1700-2300万人と言われる。慢性疼痛とは組織損傷の通常の治癒期間経過を過ぎても持続する生物学的意義のない痛みであり、中枢の可塑的変化が重要な役割を果たしている。痛みには感覚・情動・認知の成分があり、情動を司る扁桃体の可塑的変化を明らかにすることは、慢性痛の治療法を開発する上で重要である。本研究により、神経障害性疼痛の治療に用いられるプレガバリンの扁桃体への作用が、様々なモデルでシナプス増強が示されている脊髄後角から直接侵害受容性入力する経路ではなく視床皮質ネットワークからの体性感覚情報伝達経路に作用することを明らかにしたことは、慢性痛の治療を考える上で重要である。
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Report
(5 results)
Research Products
(11 results)
