Hou Bingjun
Basic Department, Shandong Medical College, Linyi, Shandong 276000, P.R. China.
Exp Ther Med. 2016 Sep;12(3):1604-1610. doi: 10.3892/etm.2016.3504. Epub 2016 Jul 5.
The administration of 100 Hz electroacupuncture has been demonstrated to suppress cocaine-induced conditioned place preference (CPP) in rats, and there is evidence that the κ-opioid receptor may have a role in cocaine addiction. The present study sought to explore the mechanisms underlying the inhibitory effects of 100 Hz electroacupuncture on cocaine-induced CPP in rats. A rat model of cocaine-induced CPP was used in the present study to investigate the following: i) Naloxone treatment (5 and 10 mg/kg) following 100 Hz electroacupuncture-mediated inhibition on cocaine-induced CPP, revealing that a high dose (10 mg/kg) of naloxone blocked the inhibitory effects of 100 Hz electroacupuncture on cocaine-induced CPP; ii) nor-binaltorphimine (nor-BNI) on 100 Hz electroacupuncture-mediated inhibition on cocaine-induced CPP, which indicated that administration of 10 µg/5 µl and 0.3 µg/1 µl nor-BNI intracerebroventricularly and via the nucleus accumbens, respectively, reversed the inhibitory effects of 100 Hz electroacupuncture on cocaine-induced CPP, and that injection of nor-BNI in different brain areas of rats blocks the inhibitory effects of electroacupuncture on cocaine-induced CPP; and iv) 100 Hz electroacupuncture on the mRNA expression levels of the κ-opioid receptor in the rat nucleus accumbens and amygdala, which established that mRNA expression levels of κ-opioid receptor in the nucleus accumbens were increased with 100 Hz electroacupuncture plus cocaine-induced CPP. Overall, the results of the present study indicated that 100 Hz electroacupuncture was able to suppress cocaine-induced CPP via the κ-opioid receptor in the nucleus accumbens.
已证明给予100赫兹电针可抑制大鼠可卡因诱导的条件性位置偏爱(CPP),且有证据表明κ-阿片受体可能在可卡因成瘾中起作用。本研究旨在探讨100赫兹电针对大鼠可卡因诱导的CPP产生抑制作用的潜在机制。本研究采用可卡因诱导的CPP大鼠模型来研究以下内容:i)100赫兹电针介导对可卡因诱导的CPP产生抑制作用后给予纳洛酮治疗(5和10毫克/千克),结果显示高剂量(10毫克/千克)的纳洛酮阻断了100赫兹电针对可卡因诱导的CPP的抑制作用;ii)去甲双氢吗啡酮(nor-BNI)对100赫兹电针介导对可卡因诱导的CPP的抑制作用,这表明分别经脑室和伏隔核给予10微克/5微升和0.3微克/1微升的nor-BNI可逆转100赫兹电针对可卡因诱导的CPP的抑制作用,并且在大鼠不同脑区注射nor-BNI可阻断电针对可卡因诱导的CPP的抑制作用;以及iv)100赫兹电针对大鼠伏隔核和杏仁核中κ-阿片受体mRNA表达水平的影响,结果确定伏隔核中κ-阿片受体的mRNA表达水平在100赫兹电针加可卡因诱导的CPP时升高。总体而言,本研究结果表明100赫兹电针能够通过伏隔核中的κ-阿片受体抑制可卡因诱导的CPP。