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Low frequency electroacupuncture (EA) analgesia has been thought to be mediated by endogenous opioids. Among other lines of evidence, it has been reported that EA stimulation delivered at 2 and 2-15 Hz in rats could be blocked or partially antagonized by naloxone (NAL) and naltrexone (NTX). In contrast, experiments in one of our laboratories (D.J.M.) showed that NAL did not inhibit 2 Hz, and even potentiated 125 Hz EA analgesia. In an attempt to resolve these discrepancies, we conducted joint experiments in the U.S.A. and in China using the methods which previously yielded NAL reversibility of EA analgesia. In no experiment did opiate antagonists block or reduce EA analgesia. On the contrary, we found that, in most experiments, NAL and NTX potentiated 2 and 2-15 Hz EA analgesia respectively. The potentiation occurred independently of laboratory methods, geographic location of the experiment, strain (Chinese or American), tail temperature, sex, and weight of rats. This potentiation suggests the existence of an opioid anti-analgesic system or that NAL and NTX acquired analgesic properties following EA. These results indicate that EA analgesia in rats is a variable phenomenon even when laboratory methods are rigorously replicated. The EA stimulation may activate multiple conflicting neural circuits which interact and ultimately modulate the analgesic outcome.