The effects of opioid receptor antagonists on electroacupuncture-produced anti-allodynia/hyperalgesia in rats with paclitaxel-evoked peripheral neuropathy.
The effects of opioid receptor antagonists on electroacupuncture-produced anti-allodynia/hyperalgesia in rats with paclitaxel-evoked peripheral neuropathy.
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DOI：
10.1016/j.brainres.2011.08.004
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发表时间：
2011-09-26
期刊：
影响因子：
2.9
通讯作者：
Zhang RX
中科院分区：
文献类型：
--
作者：
Meng X;Zhang Y;Li A;Xin J;Lao L;Ren K;Berman BM;Tan M;Zhang RX
研究支持针灸对慢性腰背和膝盖疼痛等疾病的有效性。在一项有5名患者参加的先导性研究中，该方法还改善了化疗引起的神经病理性疼痛的症状。利用已建立的紫杉醇诱导的大鼠周围神经病变模型，我们评价了电针(EA)对紫杉醇诱导的痛觉过敏和痛觉过敏的影响，这在动物模型中尚未得到研究。我们假设电针可以减轻紫杉醇引起的机械性超敏和痛敏，这是在电针后30分钟使用von Frey细丝进行评估的。从第13天开始，注射紫杉醇的大鼠对von Frey纤维(4-15g)的反应频率明显高于注射赋形剂的大鼠。与假电针相比，10 Hz电针显著降低4-15g的反应频率(p<；0.05)；100 Hz的电针仅降低15g刺激的反应频率。与假电针加载体相比，10 Hz电针加μ，δ或κ阿片受体拮抗剂均不能显著降低机械反应频率，表明三种拮抗剂均可阻断电针对痛觉过敏和痛觉过敏的抑制作用。由于我们先前在炎症性疼痛模型中证明了μ和δ而不是κ阿片受体影响电针的抗痛敏作用，这些数据表明电针在不同的条件下通过不同的阿片受体抑制疼痛。我们的数据表明，10赫兹的电针比100赫兹的电针更有效地抑制机械性痛敏/痛敏。因此，电针可通过脊髓阿片受体显著抑制紫杉醇引起的痛觉过敏，可作为神经病理性疼痛患者的辅助治疗手段。
Research supports the effectiveness of acupuncture for conditions such as chronic low back and knee pain. In a five-patient pilot study the modality also improved the symptoms of chemotherapy-induced neuropathic pain. Using an established rat model of paclitaxel-induced peripheral neuropathy, we evaluated the effect of electroacupuncture (EA) on paclitaxel-induced hyperalgesia and allodynia that has not been studied in an animal model. We hypothesize that EA would relieve the paclitaxel-induced mechanical allodynia and hyperalgesia, which was assessed 30 minutes after EA using von Frey filaments. Beginning on day 13, the response frequency to von Frey filaments (4-15 g) was significantly increased in paclitaxel-injected rats compared to those injected with vehicle. EA at 10Hz significantly (p<0.05) decreased response frequency at 4-15 g compared to sham EA; EA at 100Hz only decreased response frequency at 15 g stimulation. Compared to sham EA plus vehicle, EA at 10Hz plus either a μ, δ, or κ opioid receptor antagonist did not significantly decrease mechanical response frequency, indicating that all three antagonists blocked EA inhibition of allodynia and hyperalgesia. Since we previously demonstrated that μ and δ but not κ opioid receptors affect EA anti-hyperalgesia in an inflammatory pain model, these data show that EA inhibits pain through different opioid receptors under varying conditions. Our data indicate that EA at 10Hz inhibits mechanical allodynia/hyperalgesia more potently than does EA at 100Hz. Thus, EA significantly inhibits paclitaxel-induced allodynia/hyperalgesia through spinal opioid receptors, and EA may be a useful complementary treatment for neuropathic pain patients.
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