a Mice expressing the two transgenes were crossed and injected with tamoxifen. b Arg1 protein level was obviously reduced in the hippocampus of CX3CR1-Arg1−/− offspring compared with the Arg1f/f littermates. n = 5 per group; F1, 8 = 18.75, P < 0.001, one-way ANOVA. c Diagram of poly (I:C) insult, minocycline treatment and behavior test for CX3CR1-Arg1−/− mice and Arg1f/f littermates. d Total distance of adult offspring mice in open field test. n = 10 per group; Group: F2, 27 = 4.852, P < 0.01, two-way ANOVA. e Similar response to 70 dB background noise in the three group. n = 10 mice per group; Group: F2, 27 = 0.944, p > 0.05, two-way ANOVA. f PPI was impaired in Poly+vehicle offspring of CX3CR1-Arg1−/− mice compared to Ctrl+vehicle offspring and failed to ameliorate in Poly+Mino offspring. n = 10 mice per group; Group: F2, 27 = 10.274, P < 0.01, prepulse intensity: F2, 54 = 26.308, P < 0.001; Group × prepulse intensity: F4, 54 = 1.773, P > 0.05, three-way ANOVA with repeated measures. g Increased latency for Poly+vehicle offspring of CX3CR1-Arg1−/− mice to reach the hidden platform compared with Ctrl+vehicle offspring and failed to restore in Poly+Mino mice. n = 10 mice per group; Group: F2, 27 = 7.670, p < 0.01; day: F3, 81 = 19.035, p < 0.001; Group × day: F6, 81 = 1.553, p > 0.05; three-way ANOVA with repeated measures. h In the probe trial, data are presented as percent time and percent distance in the target quadrant. n = 10 mice per group; Group: F2, 27 = 6.298, p < 0.01, two-way ANOVA. For all figures, there is no “Genotype” or “Genotype × Group” interactions were detected (all p’s > 0.05). For Fig. g *p < 0.05, **p < 0.01, ***p < 0.001 for Poly+vehicle offspring vs. Ctrl+vehicle offspring, #p < 0.05 for Poly+Mino offspring vs. Poly+vehicle offspring. Values are the mean ± SEM. *p < 0.05, **p < 0.01, ***p < 0.001, n.s., not significant.