REVERSAL OF SPINAL-CORD NONOPIATE ANALGESIA BY CONDITIONED ANTI-ANALGESIA IN THE RAT

The spinal cord contains endogenous substances (such as cholecystokini n, FMRFamide, etc.) that can block the analgesic effects of opiates. A nti-opiate actions have been most commonly studied by exogenous admini stration of receptor agonists and receptor antagonists of these substa nces. However, we have recently demonstrated that anti-analgesia can b e brought under environmental control through Pavlovian conditioning. Whereas analgesia can be conditioned to signals for danger, anti-analg esia can be conditioned to signals for safety. Using this paradigm, we have previously demonstrated that conditioned anti-analgesia can reve rse a variety of opiate analgesic states, including those produced by conditioned danger signals, systemic morphine, and intrathecal mu- and delta-opiate receptor agonists. These data raise the question of the generality of anti-analgesia actions. The present series of experiment s examined the ability of conditioned anti-analgesia to affect non-opi ate analgesic states induced by spinal delivery of GABA(A), GABA(B), 5 HT(2) + 5HT(1), and 5HT(3) receptor agonists. While conditioned anti-a nalgesia had no effect on GABA(A) or 5HT(2) + 5HT(1) non-opiate analge sias, conditioned anti-analgesia completely blocked GABA(B) and 5HT(3) non-opiate analgesias. These findings clearly demonstrate that condit ioned anti-analgesia can powerfully modulate non-opiate as well as opi ate analgesias and bring into question whether putative anti-opiate ne uroactive substances may have broader actions than previously suggeste d. (C) 1997 International Association for the Study of Pain. Published by Elsevier Science B.V.