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脊髓 5-HT 受体参与电针对慢性疼痛的抑制作用。

Spinal 5-HT receptor is involved in electroacupuncture inhibition of chronic pain.

机构信息

Department of Physiology and Pathophysiology, School of Basic Medical Sciences, Institute of Neuroscience, Translational Medicine Institute, 12480Xi'an Jiaotong University Health Science Center, Xi'an, China.

Ministry of Education, Key Laboratory of Environment and Genes Related to Diseases (Xi'an Jiaotong University), Xi'an, China.

出版信息

Mol Pain. 2022 Jan-Dec;18:17448069221087583. doi: 10.1177/17448069221087583.

DOI:10.1177/17448069221087583
PMID:35240891
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC9006364/
Abstract

Knee osteoarthritis (KOA) is a highly prevalent, chronic joint disorder, and it is a typical disease which can develop chronic pain. Our previous study has proved that endocannabinoid (2-AG)-CB1R-GABA-5-HT pathway is involved in electroacupuncture (EA) mediated inhibition of chronic pain. However, it is still unclear which among the 5-HT receptor subtype is involved in EA evoked 5-HT mediated inhibition of chronic pain in the dorsal spinal cord. 5-HT is a G protein-coupled receptor and it is involved in 5-HT descending pain modulation system. We found that EA treatment at frequency of 2 Hz +1 mA significantly increased the expression of 5-HT receptor in the dorsal spinal cord and intrathecal injection of 5-HT receptor antagonist or agonist reversed or mimicked the analgesic effect of EA in each case respectively. Intrathecal injection of a selective GABA receptor antagonist Bicuculline also reversed the EA effect on pain hypersensitivity. Additionally, EA treatment reversed the reduced expression of GABA receptor and KCC2 in the dorsal spinal cord of KOA mice. Furthermore, we demonstrated that intrathecal 5-HT receptor antagonist/agonist reversed or mimicked the effect of EA up-regulate of KCC2 expression, respectively. Similarly, intrathecal injection of PLC and PKC inhibitors prevented both anti-allodynic effect and up-regulation of KCC2 expression by EA treatment. Our data suggest that EA treatment up-regulated KCC2 expression through activating 5-HT-Gq-PLC-PKC pathway and enhanced the inhibitory function of GABA receptor, thereby inhibiting chronic pain in a mouse model of KOA.

摘要

膝骨关节炎（KOA）是一种高发、慢性关节疾病，也是一种可发展为慢性疼痛的典型疾病。我们之前的研究已经证明内源性大麻素（2-AG）-CB1R-GABA-5-HT 通路参与了电针（EA）介导的慢性疼痛抑制。然而，在背根脊髓中，5-HT 受体亚型中哪一种参与了 EA 诱发的 5-HT 介导的慢性疼痛抑制仍然不清楚。5-HT 是一种 G 蛋白偶联受体，参与 5-HT 下行痛调制系统。我们发现，频率为 2 Hz +1 mA 的 EA 治疗显著增加了背根脊髓中 5-HT 受体的表达，鞘内注射 5-HT 受体拮抗剂或激动剂分别逆转或模拟了 EA 的镇痛作用。鞘内注射选择性 GABA 受体拮抗剂 Bicuculline 也逆转了 EA 对痛觉过敏的作用。此外，EA 治疗还逆转了 KOA 小鼠背根脊髓中 GABA 受体和 KCC2 的表达减少。此外，我们证明鞘内注射 5-HT 受体拮抗剂/激动剂分别逆转或模拟了 EA 上调 KCC2 表达的作用。同样，鞘内注射 PLC 和 PKC 抑制剂可阻止 EA 治疗的抗痛觉过敏作用和上调 KCC2 表达。我们的数据表明，EA 治疗通过激活 5-HT-Gq-PLC-PKC 通路上调 KCC2 表达，增强了 GABA 受体的抑制功能，从而抑制了 KOA 小鼠模型中的慢性疼痛。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9f97/9006364/d69734843579/10.1177_17448069221087583-fig7.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9f97/9006364/44c2741a1b80/10.1177_17448069221087583-fig1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9f97/9006364/272b4583ecab/10.1177_17448069221087583-fig2.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9f97/9006364/e7d5eea06ea1/10.1177_17448069221087583-fig3.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9f97/9006364/c8d95017691f/10.1177_17448069221087583-fig4.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9f97/9006364/f8873be85a22/10.1177_17448069221087583-fig5.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9f97/9006364/e76b36fd63c2/10.1177_17448069221087583-fig6.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9f97/9006364/d69734843579/10.1177_17448069221087583-fig7.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9f97/9006364/44c2741a1b80/10.1177_17448069221087583-fig1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9f97/9006364/272b4583ecab/10.1177_17448069221087583-fig2.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9f97/9006364/e7d5eea06ea1/10.1177_17448069221087583-fig3.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9f97/9006364/c8d95017691f/10.1177_17448069221087583-fig4.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9f97/9006364/f8873be85a22/10.1177_17448069221087583-fig5.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9f97/9006364/e76b36fd63c2/10.1177_17448069221087583-fig6.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9f97/9006364/d69734843579/10.1177_17448069221087583-fig7.jpg

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