Bradykinin into amygdala induces thermal hyperalgesia in rats.

摘要: Abstract Bradykinin is one of the most potent endogenous algesic substances and its role in pain transmission has been intensively studied periphery. However, action this peptide central structures involved remains unclear. Administration bradykinin (0.25 nmol/site) into right amygdala adult male Wistar rats induced thermal hyperalgesia, evaluated paw-flick test. Bradykinin-induced hyperalgesia was abolished by co-administration with B2 receptor antagonist Hoe 140 (5 pmol/site), NMDA MK-801 (5 nmol/site), cyclooxygenase inhibitor indomethacin (10 nmol/site) glial metabolic fluorocitrate (1 nmol/site). Since intra-amygdala administration did not alter spontaneous locomotion open-field test, it unlikely that current described hyperalgesic effect due to an unspecific on motor activity. These findings provide evidence bradykinin, through activation amygdalar receptors induces glutamatergic- prostanoid-mediated mechanisms are such effect.