Olfactory memory experiments with GluR-BRescue , and both GluR-BΔFB and GluR-B2lox mice as controls, were performed as described above (indicated with shaded symbols in Figure 6A). Memory was again highly reproducible in both GluR-BΔFB (66 ± 12%; n = 4) and GluR-B2lox (94 ± 2%; n = 3) mice, compared with experiments performed earlier (Figures 2E and 4A). Importantly, olfactory memory in GluR-BRescue mice was intermediate (75 ± 15%, n = 8), below GluR-B2lox control levels, but better than in GluR-BΔFB mice. Assessing memory under extinction-free condition, where each trial was rewarded, confirmed again that the memory deficit was a true memory deficit and not due to increased extinction (Figure S3B). Data from the experiments described in Figures 2 and 4 were combined to allow statistical comparison (Figure 6A and 6B). In summary, GluR-BRescue mice showed both enhanced memory performances compared with GluR-BΔFB (overall ANOVA: F(2,41) = 13.6, p < 10−4; memoryRescue = 75 ± 15%, n = 8; memoryΔFB = 66 ± 14%, n = 22; p < 0.05; Figure 6A), but were still impaired relative to GluR-B2lox controls (memory2lox = 88 ± 8%, n = 14; p < 0.005), consistent with a partial rescue of the memory deficit by circumscribed transgenic GFPGluR-B expression in hippocampus and piriform cortex. Notably, the partial memory is in numerical agreement with the predictions from the protein correlation and the measurement of transgenic protein expression (see predicted memory, blue line, in Figure 6B). In the olfactory memory experiments with GluR-BΔFB animals, olfactory memory linearly depended on GluR-B expression in cortex and hippocampus with a slope of 9.1 ± 2.5% (cortex) and 8.9 ± 2.0% (hippocampus) increase in memory per 10% increase in protein (Figure 4D). A 9.7% increase in GluR-B in these brain regions, as achieved by GluR-BRescue animals (Figure 5), is thus predicted to increase olfactory memory by approximately 9% throughout the heterogeneous population (blue line in Figure 6B). This confirms the role of these brain areas as inferred from the mosaic expression and protein correlation analysis described above (Figure 4). However, odor discrimination (measured by the discrimination index as in Figures 1, 2, and 4D) was as enhanced as in GluR-BΔFB mice (0.79 ± 0.05, mean ± SEM compared with 0.76 ± 0.02, p > 0.7, Figure 6C), and improved relative to GluR-B2lox controls (0.48 ± 0.06; Figure 6C; overall ANOVA: F(2,41) = 17.2, p < 10−5; post hoc Newman Keuls: p < 10−3), as expected if the enhanced discrimination phenotype is due to Ca2+-permeable AMPARs in the olfactory bulb and unaffected by GluR-B expression in piriform cortex or hippocampus.