Tifluadom (KC 5103) induces suppression and latency changes on somatosensory evoked potentials which are reversed by opioid antagonists.
Suppression of evoked potentials of the EEG are indicators of analgesia. Tifluadom induces latency changes which are reversed by the kappa-antagonist Mr 2266. Naloxone reverses peak suppression which indicates an additional interaction with the my-opioid-receptor. The specific benzodiazepine antagonist Ro 15-1788 is not effective in reversing peak-changes. Therefore nociceptive stimuli are modulated by tifluadom not only through the interaction with kappa- but also with my-opioid-receptors.
D000818:Animals; D001569:Benzodiazepines / Q000494:pharmacology*; D002540:Cerebral Cortex / Q000187:drug effects / Q000502:physiology*; D004285:Dogs; D004336:Drug Antagonism; D004558:Electric Stimulation; D005073:Evoked Potentials, Somatosensory / Q000187:drug effects*; D008475:Median Nerve / Q000502:physiology; D009292:Narcotic Antagonists / Q000494:pharmacology*; D011957:Receptors, Opioid / Q000187:drug effects*
D009292:Narcotic Antagonists; D011957:Receptors, Opioid; D001569:Benzodiazepines; C035470:tifluadom