In agreement with the results of other authors, rats sensitized to morphine and challenged with 5 mg/kg of morphine after 7 days of wash-out showed intense stereotyped movements, the expression of which was selectively antagonized by SCH 23390. Sensitized rats were exposed to an unavoidable stress (which consistently produces an escape deficit in control animals) after 3, 7 and 21 days of morphine wash-out. Twenty-four hours after the unavoidable stress, animals were tested for their capacity to escape and their performance was compared to that of control-stressed and naive rats. Morphine sensitization completely prevented the development of escape deficit. This protective effect was similar to that induced by a chronic imipramine treatment and, like the effect of imipramine, it was antagonized by the administration of SCH 23390 before the unavoidable stress. However, it was not affected by the administration of naloxone. Moreover, when rats presenting a clear-cut escape deficit, induced by a 10-day treatment with SKF 38393, were exposed to the morphine sensitization protocol, a complete recovery of their capacity to avoid a noxious stimulus was observed. Finally, the down-regulation of both the number of D(1)-dopamine receptors and of the coupled adenylyl cyclase activity in the pre-frontal cortex (PFC) produced by long-term SKF 38393 administration was reverted by the superimposed morphine sensitization. Thus, the condition of morphine sensitization appears to share several common effects with chronic imipramine treatment.