Bossut D F, Mayer D J
Department of Physiology, Medical College of Virginia, Virginia Commonwealth University, Richmond 23298.
Brain Res. 1991 May 17;549(1):47-51. doi: 10.1016/0006-8993(91)90597-o.
Inhibition of pain by low frequency electroacupuncture (EA) has been thought to be mediated by endogenous opioids. We reported in a previous paper, however, that naloxone (NAL) and naltrexone (NTX) either potentiated or had no effect on analgesia in EA-naive rats, independent of origin (American or Chinese), sex, weight, geographic location (the U.S.A. or China), or numerous variations of experimental methodology. In the present study, we hypothesized that the number of exposures to EA treatment may be responsible for the discrepant effect of opiate antagonists. We found, as previously demonstrated, analgesia in EA-naive rats was potentiated by NTX. After two pre-exposures to EA, however, NTX antagonized analgesia. These results indicate that, in rats: (1) pre-exposure is a key variable for opiate antagonists to produce antagonism or potentiation of analgesia; (2) environmental cues paired with the initial analgesic manipulation may be responsible for converting analgesia from non-opioid to opioid, as already demonstrated with classically conditioned and learned helplessness induced analgesia; and (3) EA analgesia in rats is a multidimensional manipulation which can be influenced by subtle environmental changes.
低频电针（EA）对疼痛的抑制作用被认为是由内源性阿片类物质介导的。然而，我们在之前的一篇论文中报道，纳洛酮（NAL）和纳曲酮（NTX）对未接受过EA处理的大鼠的镇痛作用要么有增强作用，要么没有影响，这与大鼠的来源（美国或中国）、性别、体重、地理位置（美国或中国）或实验方法的众多变化无关。在本研究中，我们假设接受EA治疗的次数可能是阿片类拮抗剂产生不同作用的原因。正如之前所证明的，我们发现NTX增强了未接受过EA处理的大鼠的镇痛作用。然而，在对EA进行两次预先暴露后，NTX拮抗了镇痛作用。这些结果表明，在大鼠中：（1）预先暴露是阿片类拮抗剂产生镇痛拮抗或增强作用的关键变量；（2）与最初的镇痛操作配对的环境线索可能是导致镇痛作用从非阿片类转变为阿片类的原因，这已在经典条件反射和习得性无助诱导的镇痛中得到证明；（3）大鼠的EA镇痛是一种多维操作，可能会受到细微环境变化的影响。
