Background: While the most widely known function of renin angiotensin system (RAS) is related to cardiovascular regulation, evidence also suggests an important role of RAS in the response to emotional stress. Our previous studies in a mouse model of PTSD have shown that peripheral AT1R inhibition with losartan increases the extinction (learned inhibition) of a traumatic fear memory and this affects brain AT1R mRNA expression. Therefore the purpose of this study was to further investigate brain RAS in the consolidation of fear memory. Methods: We performed classical Pavlovian fear conditioning in mice pairing auditory cues with foot shocks and examined mRNA expression of components of brain RAS and examined fear extinction behavior (% freezing to conditioned stimulus). Results: Following the acquisition of fear, there was a 5 fold and 3 fold increase (*p <0.05, n=6) in mRNA expression of AT2R and angiotensin converting enzyme 2 (ACE2) in the central amygdala (CeA) and bed nucleus stria terminalis (BNST), regions involved in the consolidation of fear memory. However, mRNA expressions of the classical RAS pathway (AT1R and ACE) were unaltered in these brain regions. Thus we examined the effect of AT2R on long-term fear memory. Mice received intraparietal (IP) or intracerebral (ICV) injections of either the novel non-peptide AT2R -agonist, Compound 21 (C21), or AT2R antagonist PD123,319 (PD) during classical Pavlovian fear conditioning. Twenty-four hours following fear conditioning both C21 (10 mg/kg IP or 2µg/kg ICV) and PD (15 mg/kg IP or 200 µg/kg ICV) had no effect on extinction of fear memory compared to the vehicle. However, when fear memory retention was tested, the ICV C21 treated mice exhibited a trend for decreased freezing (C21 – 38%) (t(15) = 1.7; p = 0.1) versus saline (55%) and PD (64%) injected animals. Conclusion: These data suggest that brain AT2Rs and ACE 2 may play a role in fear memory formation and / or retrieval. Future studies are required to understand the differential regulation of brain angiotensin receptor signaling and the implications for the treatment of PTSD. Values are means ± S.E.M., compared by ANOVA