Exposure to stresses, nociceptive or non-nociceptive stress, induce antinociceptive effect (stress-induced analgesia: SIA) in experimental animals. The underlaying mechanism for their induction depend on the nature of the stresses, mediated via various kind of neurotransmitter receptors such as opioid-, catecholamine- and benzodiazepin-receptors, and adrenal cortical hormone and brain vasopressin also play a role in the mechanisms. The development of tolerance to the analgesic effect of morphine was blocked by FS or PSY stress, but not by SW stress, as far as the concomitant treatment with morphine was continued without affecting the analgesic effect and the development of physical dependence. These phenomena are consistent with the fact that development of tolerance and/or dependence to opioid is not apparent in the patients suffering from severe pain, and also may suggest the possible dissociation of analgesic effect, tolerance and dependence of morphine by the underlying mechanism. On the other hand, it is suggested that the processes of the development of tolerance to opioid and the formation of learning/memory are underlaid with a common mechanism, for instance, both phenomena are blocked by the pretreatment with protein synthesis inhibitors, such as cycloheximide, puromycin and actinomycin D. In the experiments using one-trial step-through type passive avoidance learning task, exposure of mice to FS, SW and PSY stress at various time, pre-, post-training and pre-test, produced diverse effects in the test trial latencies, facilitation by pre-, post-training, pre-test FS and pre-training PSY, impairment by post-training SW, depending on the timing of exposure and the character of their acute effect. Precise analysis of the mechanism of these discrepancies may lead to the clarification of the biological regulatory mechanism when the living organism are exposed to the nociceptive stresses.