Ago2 is dispensable for brain organization and neuronal maintenance in the adult brain. (A) Conditional inactivation of Ago2 in adult neurons. Expression of Ago2 was analyzed by Western blotting of the striatal protein lysates derived from three Ago2^fl/fl mice (lanes 1–3), and three Camk2a-Cre; Ago2^fl/fl mice (lanes 4–6). The lysates derived from Ago2^−/− and WT mouse embryonic fibroblasts (MEF) were used as controls for the specificity of the anti-Ago2 antibodies. Equal protein concentration in the samples was controlled by β actin loading. (B and C) Ago2 deficiency in the forebrain does not affect brain morphology. (B) The overall brain morphology of 12-wk-old Camk2a-Cre; Ago2^fl/fl and Ago2^fl/fl control mice was analyzed using standard Nissl-stain (n = 3/genotype). Two representative images from sagittal brain sections of mice of both genotypes are shown. (C) Saggital brain sections of Ago2^fl/fl and Camk2a-Cre; Ago2^fl/fl mice are shown (n = 3/genotype). Striatal morphology was analyzed by visualizing Drd1 and Drd2 MSNs (top) using antibodies against the MSN-enriched protein DARPP-32 (green) and the Drd2-MSN–specific adenosine 2A (A2A) receptor (red); the dopaminergic terminals (bottom) were visualized by expression of the dopamine-producing enzyme TH (green), and neuronal nuclei in the striatum were visualized by using the neuron-specific marker NeuN (red). The nucleus of each cell was visualized using Draq5 DNA staining (blue). Bar, 100 µm.