The interpretation of “antianalgesia” systems needs reexamination

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I n their paper, Maier and colleagues proposed the existence of an “antianalgesia” system triggered by “safety” signals and mediated by the release of cholecystokinin (CCK) in the spinal cord. They also proposed the existence of a hyperalgesia system activated by illness. These proposals are fascinating, and there is no doubt that they will lead to extensive experimental investigation in both animals and humans. This new insight in the domain of pain modulation reminds us of the initial enthusiastic studies of the 1970s related to the stimulation-producing analgesia phenomenon. In fact, until the end of the 1980s the use of deep brain stimulation in the relief of intractable pain in humans seemed to be effective according to various neurosurgical groups. However, actually, this technique is less and less used, notably in Europe, and the controversies concerning it are wellexplained by the numerous side effects obtained by periaqueductal gray electrical stimulation in the rat9,” This was a good illustration of how the results collected by different groups in behavioral research are sometimes not homogeneous and that extensive interpretation may sometimes be premature. In this respect, Maier and colleagues, with great prudence, wrote that “the suggestions made in this paper are tentative,” and they indicated that “they are going well beyond the data.” The most exciting finding of this article, which has triggered such enthusiasm and lack of moderation, was that a “safety” signal was able to reduce morphine analgesia when the opiate effects were gauged by means of the tail-flick test and given systemically