Strain and sex differences in the expression of nociceptive behavior and stress-induced analgesia in rats.

Evidence indicates that genetic, gender, and emotional/attentional aspects modulate the pain sensation. The present study examined the effect of swim-stress on nociceptive responses in Lewis (LEW) and spontaneously hypertensive (SHR) inbred rats (contrasting for anxiety-related behaviors), as well as in Wistar (WIS) rats of both sexes. Furthermore, we explored possible neurochemical mechanisms involved. In addition, we investigated whether habituation in the hot-plate apparatus could modify the hypoalgesic phenotype of SHR. Male and female LEW, SHR, and WIS rats were tested immediately before and 2 min after a 3-min swim in 15 degrees C water. The swim-stress induced analgesia in LEW and WIS, but not in SHR male rats. The same stressor induced analgesia in females of all three strains. In WIS female rats, the stress-induced analgesia (SIA) seems to involve, at least partially, a nonopioid N-methyl-d-aspartate (NMDA) analgesic system. Moreover, five brief exposures (90 s; 10-min intertrial interval) to the unheated hot-plate apparatus completely abolished the differences in basal hot-plate latencies observed in SHR compared with LEW and WIS strains. The present results demonstrate genetic and gender differences in nociceptive sensitivity and in the activation of endogenous analgesic systems in rats and highlight the influence of emotional reactivity. The SHR's hypoalgesic phenotype seems to involve central cognitive processes. Therefore, the LEW and SHR inbred strains may provide an important tool for study of the molecular bases underlying nociception and its modulation and the relationship with emotional/attentional processes.