Abstract
Our recent investigations demonstrated that microinjections of three nonsteroidal anti-inflammatory drugs (NSAIDs), Analgin, ketorolac, or xefocam, into the central nucleus of the amygdala produce tolerance to these drugs and cross-tolerance to morphine. We observed the same phenomenon in the midbrain periaqueductal gray matter. In this report, we show that microinjections of NSAIDs into the nucleus raphe magnus (NRM) produces antinociception, as indicated by latency increases in both tail-flick (TF) and hot-plate (HP) reflexes compared to controls with saline microinjected into the same nucleus. Furthermore, microinjection of the μ-opioid antagonist naloxone into the NRM significantly decreased antinociceptive effects of NSAIDs characterized by the TF and HP latencies on the 1st experimental day. On the 2nd day, naloxone also provided some trend effects in both TF and HP tests. These results strongly support the suggestion that the endogenous opioid system is significantly involved in NSAID-induced antinociception and tolerance.
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