Endogenous opioid and cannabinoid systems contribute to antinociception produced by administration of NSAIDs into the insular cortex of rats.

Pain sensation is characterized as a complex experience, dependent on sensory processes as well as the activation of limbic brain areas involved in emotion, among them anterior insula. This cortical area is involved in the perception and response to painful stimuli. We investigated if this area contributes to antinociception produced by NSAIDs, and underlying mechanisms.

NALOXONE AND CTOP BLOCK NSAIDS-INDUCED ANTINOCICEPTION IN ANTERIOR CINGULATE CORTEX OF RATS.

Anterior cingulate cortex (ACC), which is activated by noxious stimuli, is involved in pain processing, the neural mechanisms of the ACC involvement in affective pain have yet to be elaborated. To study relation antinociceptive effects induced by non-steroidal anti-inflammatory drugs (NSAIDs) with endogenous opioid system we treated experimental rats with opioid receptor antagonists, naloxone and CTOP in the ACC pre- and post-following microinjections with NSAIDs. We measured nociceptive thermal paw withdrawal latencies and mechanical thresholds in rats' formalin test following microinjections of NSAIDs (diclofenac, ketoprofen, ketorolac and lornoxicam), saline or opioid receptor antagonists, naloxone and CTOP in the ACC.

ANTINOCICEPTIVE TOLERANCE TO NSAIDS PARTIALLY MEDIATED VIA ENDOCANNABINOIDS IN ANTERIOR CINGULATE CORTEX OF RATS.

Pain is characterized as a complex experience, dependent not only on the regulation of nociceptive sensory systems but also on the activation of mechanisms that control emotional processes in limbic brain areas. Non-opioid, non-steroidal anti-inflammatory drugs (NSAIDs) are the most widely used analgesics in the treatment of not-severe pain. We have recently shown that repeated doses result in tolerance to these drugs like opioids.