Figure 3.
Genetic inactivation of adenosine A2A receptors prevents β-amyloid-induced synaptotoxicity and memory impairment. Wild-type C57BL/6 or A2AR KO mice were treated with Aβ1-42 (2 nmol, i.c.v.) or water [control (CTR)] and analyzed after 15 d. A, B, Spontaneous alternation in the Y-maze test (A) and spontaneous locomotion evaluated in an open-field arena (B) (data are mean ± SEM of n = 7 mice per experimental group; *p < 0.001). C, Western blot comparing synaptophysin and SNAP-25 immunoreactivity in hippocampal membranes obtained from wild-type or A2AR KO mice injected with water (CTR) or Aβ1-42 (data are mean ± SEM of n = 4 mice per experimental group; *p < 0.001). D, Fluoro-Jade C staining of neuronal death, CD11-b immunohistochemistry evaluating microgliosis, and GFAP immunohistochemistry evaluating astrogliosis in hippocampal sections from wild-type or A2AR KO mice injected with water (CTR) or Aβ1-42 (images representative of n = 4 mice per experimental group).