Bacitracin produces analgesia by increasing brain immunoreactive beta-endorphin (beta-E) content.

The effects of protease inhibitor bacitracin on brain beta-endorphin content and analgesia, were examined in vivo. Male Sprague-Dawley rats were injected with bacitracin intracerebroventricularly and sacrificed by microwave irradiation 15 and 30 min after injection. Brain beta-endorphin levels were 27% higher in bacitracin treated rats than in controls. A second group of bacitracin injected rats was subjected to continuous intermittent 55 degrees C hot plate exposure. Bacitracin-injected rats exhibited total analgesia 15 min after bacitracin injection. At 30 min, this analgesic effect subsided. Control rats exhibited no analgesia. Bacitracin induced analgesia was naloxone reversible at a low dose of naloxone (1 mg/kg). At a higher dose of naloxone (10mg/kg), bacitracin induced analgesia was only partially antagonized. These results suggest that bacitracin induced analgesia might be due to the elevated levels of brain beta-endorphin caused by a decrease in its breakdown by bacitracin.