Electroacupuncture suppresses capsaicin-induced secondary hyperalgesia through an endogenous spinal opioid mechanism.
Electroacupuncture suppresses capsaicin-induced secondary hyperalgesia through an endogenous spinal opioid mechanism.
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DOI：
10.1016/j.pain.2009.06.035
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发表时间：
2009-10
期刊：
影响因子：
7.4
通讯作者：
Chung JM
中科院分区：
文献类型：
--
作者：
Kim HY;Wang J;Lee I;Kim HK;Chung K;Chung JM
由组织炎症或外周神经损伤引起的中枢敏感化在持续性疼痛中起重要作用。辣椒素诱发疼痛的动物模型具有明确的外周和中枢致敏成分，因此可用于研究对两种单独成分的镇痛作用。本研究的重点是研究电针对辣椒素引起的继发性痛敏的镇痛作用。将辣椒素（0.5%，10 μl）注射到左后爪的足底侧，并测定大鼠对von Frey刺激（机械敏感性）的缩足阈值，用于原发性和继发性痛觉过敏。在异氟醚麻醉下，电针（2 Hz，3 mA）于不同的穴位对（GB 30-GB 34，BL 40-BL 60，GV 2-GV 6，LI 3-LI 6和SI 3-TE 8）30 min，然后测定电针对爪机械敏感性的影响。电针同侧SI 3-TE 8穴可显著降低辣椒素诱发的继发性痛敏，但对原发性痛敏无显著影响。电针镇痛作用可被全身性非特异性阿片受体（OR）拮抗剂或鞘内μ-或δ-OR拮抗剂抑制。EA镇痛作用不受鞘内κ-OR拮抗剂或全身肾上腺素能受体拮抗剂的影响。电针对辣椒素诱发的继发性痛觉过敏（中枢敏感化）具有刺激点特异性镇痛作用，其机制可能是通过激活脊髓内源性μ和δ阿片受体介导的。
Central sensitization, caused either by tissue inflammation or peripheral nerve injury, plays an important role in persistent pain. An animal model of capsaicin-induced pain has well-defined peripheral and central sensitization components, thus is useful for studying the analgesic effect on two separate components. The focus of this study is to examine the analgesic effects of electroacupuncture (EA) on capsaicin-induced secondary hyperalgesia, which represents central sensitization. Capsaicin (0.5%, 10 μl) was injected into the plantar side of the left hind paw, and foot withdrawal thresholds in response to von Frey stimuli (mechanical sensitivity) were determined for both primary and secondary hyperalgesia in rats. EA (2 Hz, 3 mA) was applied to various pairs of acupoints, GB30-GB34, BL40-BL60, GV2-GV6, LI3-LI6 and SI3-TE8, for 30 min under isofluraine anesthesia and then the effect of EA on mechanical sensitivity of paw was determined. EA applied to the ipsilateral SI3-TE8, but none the other acupoints, significantly reduced capsaicin-induced secondary hyperalgesia but not primary hyperalgesia. EA analgesic effect was inhibited by a systemic non-specific opioid receptor (OR) antagonist or an intrathecal μ- or δ-OR antagonist. EA analgesic effect was not affected by an intrathecal κ-OR antagonist or systemic adrenergic receptor antagonist. This study demonstrates that EA produces a stimulation point specific analgesic effect on capsaicin-induced secondary hyperalgesia (central sensitization), mediated by activating endogenous spinal μ and δ opioid receptors.
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影响因子：
2.9
作者：
CODERRE, TJ;MELZACK, R
通讯作者：
MELZACK, R
影响因子：
4.3
作者：
Gopalkrishnan, P;Sluka, KA
通讯作者：
Sluka, KA
影响因子：
4
作者：
King, EW;Sluka, KA
通讯作者：
Sluka, KA
影响因子：
2.5
作者：
BAUMANN, TK;SIMONE, DA;LAMOTTE, RH
通讯作者：
LAMOTTE, RH
DOI：
10.1046/j.1440-1681.2001.03561.x
发表时间：
2001-12-01
影响因子：
2.9
作者：
Barrès, C;Neto, EPD;Julien, C
通讯作者：
Julien, C