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The bradykinin (BK) receptors B1R and B2R are involved in inflammatory responses and their activation can enhance tissue damage. The B2R is constitutively expressed and mediates the physiologic effects of BK, whereas B1R expression is induced after tissue damage. Recently, they have been involved with Alzheimer’s disease, ischemic stroke and traumatic brain injury (TBI). In this study, we investigated the role of bradykinin in short and long-term memory consolidation (STM and LTM). It was observed that bilateral injection of BK (300 pmol/μl) disrupted the STM consolidation but not LTM, both evaluated by inhibitory avoidance test. The STM disruption due to BK injection was blocked by the previous injection of the B1R antagonist des-Arg 10 -HOE140 but not by the B2R antagonist HOE140. Additionally, the injection of the B1 agonist desArg 9 -BK disrupted STM and LTM consolidation at doses close to physiological concentration of the peptide (2.3 and 37.5 pmol, respectively) which could be reached during tissue injury. The presence of B1R located on glial cells around the implanted guide cannula used for peptide injection was confirmed by immunofluorescence. These data imply in a possible participation of B1R in the STM impairment observed in TBI, neuroinflammation and neurodegeneration.

Kinin B1 receptor mediates memory impairment in the rat hippocampus