Center for Integrative Medicine, School of Medicine, University of Maryland, 685 W Baltimore street, MSTF Rm 8-22, Baltimore, MD 21201, USA.
Neurochem Res. 2011 Oct;36(10):1785-92. doi: 10.1007/s11064-011-0495-1. Epub 2011 May 10.
We previously showed that electroacupuncture (EA) activates medulla-spinal serotonin-containing neurons. The present study investigated the effects of intrathecal 5,7-dihydroxytryptamine creatinine sulfate, a selective neurotoxin for serotonergic terminals, the 5-hydroxytryptamine 1A receptor (5-HT1AR) antagonist NAN-190 hydrobromide and the 5-HT2C receptor (5-HT2CR) antagonist SB-242,084 on EA anti-hyperalgesia. EA was given twice at acupoint GB30 after complete Freund's adjuvant (CFA) injection into hind paw. CFA-induced hyperalgesia was measured by assessing hind paw withdrawal latency (PWL) to a noxious thermal stimulus 30 min post-EA. Serotonin depletion and the 5-HT1AR antagonist blocked EA anti-hyperalgesia; the 5-HT2CR antagonist did not. Immunohistochemical staining showed that spinal 5-HT1AR was expressed and that 5-HT2CR was absent in naive and CFA-injected animals 2.5 h post-CFA. These results show a correlation between EA anti-hyperalgesia and receptor expression. Collectively, the data show that EA activates supraspinal serotonin neurons to release 5-HT, which acts on spinal 5-HT1AR to inhibit hyperalgesia.
我们之前的研究表明,电针(EA)可以激活含有脊髓血清素的神经元。本研究旨在探讨鞘内给予 5,7-二羟基色胺肌酸硫酸盐(一种选择性的血清素末端神经毒素)、5-羟色胺 1A 受体(5-HT1AR)拮抗剂 NAN-190 氢溴酸盐和 5-羟色胺 2C 受体(5-HT2CR)拮抗剂 SB-242,084 对 EA 抗痛觉过敏的影响。在向足底注射完全弗氏佐剂(CFA)后,在穴位 GB30 处给予两次 EA。通过评估 EA 后 30 分钟对有害热刺激的后足撤回潜伏期(PWL)来测量 CFA 诱导的痛觉过敏。血清素耗竭和 5-HT1AR 拮抗剂阻断了 EA 抗痛觉过敏;5-HT2CR 拮抗剂则没有。免疫组织化学染色显示,在 CFA 注射后 2.5 小时,脊髓 5-HT1AR 表达,而 5-HT2CR 在未处理和 CFA 注射动物中均不存在。这些结果表明 EA 抗痛觉过敏与受体表达之间存在相关性。总的来说,这些数据表明,EA 激活了中枢血清素神经元以释放 5-HT,5-HT 作用于脊髓 5-HT1AR 以抑制痛觉过敏。