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    Please use this identifier to cite or link to this item: http://ir.lib.ncu.edu.tw/handle/987654321/75254

    Title: Peripheral 5-HT3 participates in mediating mirror-image pain by a cross-talk with ASIC3
    Authors: 蘇禹軒;Su, Yeu-Shiuan
    Contributors: 生命科學系
    Keywords: 鏡像疼痛;發炎性疼痛;血清素受體3;酸敏感離子通道;mirror-image pain;inflammatory pain;5-HT3 receptor;ASIC3;cross-talk
    Date: 2017-12-11
    Issue Date: 2018-01-16 10:22:22 (UTC+8)
    Publisher: 國立中央大學
    Abstract: 當組織受傷或發炎的時候,許多內源性的介質包括:前列腺素(PGE2)、血清素(5-HT)、氫離子、組織胺(Histamine)、三磷酸腺苷(ATP),會從這些部位的組織或免疫細胞釋出,誘導發炎和傷害感受的產生。5-HT是一種發炎的介質,參與調控發炎性疼痛。在週邊和中樞痛覺神經元上存在許多5-HT受體的亞型,因此研究5-HT在疼痛中的作用也相對複雜。在之前的研究中,我們發現5-HT2B/2C受體的拮抗劑可以抑制由5-HT所誘導的機械性痛覺敏感。然而,造成這種痛覺敏感所影響的神經元類型以及訊號路徑,仍然還不清楚。本篇論文的第一個部分,我證明了5-HT2B受體透過調控Gq /11β-蛋白質激酶C(PKCε)的途徑參與5-HT在小鼠中所誘導的機械性痛覺敏感。注射TRPV1的拮抗劑抑制了5-HT所造成的機械性痛覺敏感現象;而TRPV1基因剔除的小鼠在注射5-HT後也得到相同的結果。因此,5-HT2B受體透過調控TRPV1的功能,參與在血清素所引發的機械性痛覺敏感現象。
    ;The endogenous mediators, such as prostaglandin E2 (PGE2), bradykinin (BK), serotonin [5-hydroxytryptamine (5-HT)], proton, histamine, and ATP, are released from the damaged site of the tissue and immune cells to induce inflammation and nociception. 5-HT, an inflammatory mediator, contributes to inflammatory pain. The presence of multiple 5-HT subtype receptors on peripheral and central nociceptors complicates the role of 5-HT in pain. Previously, we found that 5-HT2B/2C antagonist blocks 5-HT-induced mechanical hyperalgesia. However, the types of neurons or circuits underlying this effect remained unsolved. In the first part of this thesis, I demonstrate that the Gq/11β-protein kinase Cε (PKCε) pathway mediated by 5-HT2B is involved in 5-HT-induced mechanical hyperalgesia in mice. Administration of a transient receptor potential vanilloid 1 (TRPV1) antagonist inhibited the 5-HT-induced mechanical hyperalgesia. Similar results were found in TRPV1-deficient mice. Thus, 5-HT2B mediates 5-HT-induced mechanical hyperalgesia by regulating TRPV1 function.

    In the second part of the theis, I focus on mirror-image pain (MIP), which occurs along with complex regional pain syndrome, rheumatoid arthritis and chronic migraine, is characterized by increased pain sensitivity of healthy body regions other than the actual injured or inflamed sites. A high level of peripheral inflammation may activate central or peripheral glia, triggering mirror-image pain. However, which receptors mediate inflammatory signals to contribute glial activation remains unclear. Intraplantarly injecting mice with 5-HT or acidic buffer (proton) caused only unilateral hyperalgesia, but co-injection of 5-HT/acid induced bilateral hyperalgesia (MIP). Blocking 5-HT3 or acid-sensing ion channel 3 (ASIC3) abolished satellite glial activation, inhibiting MIP. Interestingly, intraplantar administration of a 5-HT3 agonist induced MIP, and 5-HT3–mediated MIP can be reversed by a 5-HT3 antagonist or an ASIC3 blocker. Similar results were found using ASIC3 agonist. Furthermore, 5-HT3 was observed to co-localize with ASIC3 in DRG neurons; 5-HT3 activation induced an increase in intracellular calcium that was inhibited by an ASIC3 blocker and vice versa. A cross-talk between 5-HT3 and ASIC3 mediates satellite glial activation, thereby triggering mirror-image pain.
    Appears in Collections:[生命科學研究所 ] 博碩士論文

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