Helmholtz Gemeinschaft


Angiotensin-(1-7)/Mas axis integrity is required for the expression of object recognition memory

Item Type:Article
Title:Angiotensin-(1-7)/Mas axis integrity is required for the expression of object recognition memory
Creators Name:Lazaroni, T.L.N. and Raslan, A.C.S. and Fontes, W.R.P. and de Oliveira, M.L. and Bader, M. and Alenina, N. and Moraes, M.F.D. and Dos Santos, R.A. and Pereira, G.S.
Abstract:It has been shown that the brain has its own intrinsic renin-angiotensin system (RAS) and angiotensin-(1-7) (Ang-(1-7)) is particularly interesting, because it appears to counterbalance most of the Ang II effects. Ang-(1-7) exerts its biological function through activation of the G-protein-coupled receptor Mas. Interestingly, hippocampus is one of the regions with higher expression of Mas. However, the role of Ang-(1-7)/Mas axis in hippocampus-dependent memories is still poorly understood. Here we demonstrated that Mas ablation, as well as the blockade of Mas in the CA1-hippocampus, impaired object recognition memory (ORM). We also demonstrated that the blockade of Ang II receptors AT1, but not AT2, recovers ORM impairment of Mas-deficient mice. Considering that high concentrations of Ang-(1-7) may activate AT1 receptors, nonspecifically, we evaluate the levels of Ang-(1-7) and its main precursors Ang I and Ang II in the hippocampus of Mas-deficient mice. The Ang I and Ang II levels are unaltered in the whole hipocampus of MasKo. However, Ang-(1-7) concentration is increased in the whole hippocampus of MasKo mice, as well as in the CA1 area. Taken together, our findings suggest that the functionality of the Ang-(1-7)/Mas axis is essential for normal ORM processing.
Keywords:Angiotensin-(1-7), Receptor Mas, Object Recognition Memory, AT1 Receptor, Animals, Mice
Source:Neurobiology of Learning and Memory
Publisher:Elsevier / Academic Press
Page Range:113-123
Date:January 2012
Official Publication:https://doi.org/10.1016/j.nlm.2011.10.003
PubMed:View item in PubMed

Repository Staff Only: item control page

Open Access
MDC Library