Figure 3.

Additive effects between prenatal immune activation and Nurr1 deficiency in the development of sensorimotor gating deficiency. Pregnant wt and Nurr1^+/− mice were treated with the viral mimetic poly(I:C) (POL) (2 mg/kg, i.v.) or vehicle [saline (SAL)] on gestation day 17, and the resulting offspring were tested in early adulthood. Sensorimotor gating was assessed by PPI of the acoustic startle reflex. A, The line plot shows percentage PPI as a function of three different pulse intensities (P-100, P-110, and P-120, which correspond to 100, 110, and 120 dB_A) and prepulse intensities (+6, +12, and +18 dB_A above background of 65 dB_A); the bar plot depicts the mean percentage PPI across all prepulse and pulse stimuli used. Percentage PPI was calculated by the following expression: 100% × [1 − (mean reactivity on prepulse-plus-pulse trials/mean reactivity on pulse-alone trials)], for each subject, and at each of the three possible pulse and prepulse intensities. *p < 0.05 and ^§p < 0.05, reflecting the main effects of genotype and prenatal treatment, respectively. N = 14 in each experimental group; all values are means ± SEM. B, The line plot shows startle reactivity (in arbitrary units) to pulse-alone trials as a function of the three different pulse intensities (100, 110, and 120 dB_A), and the bar plot depicts the mean startle reactivity across all pulse stimuli used. *p < 0.05, signifying the significant difference between POL-exposed Nurr1^+/− mice and all other groups. N = 14 in each experimental group; all values are means ± SEM. C, Raw score analysis of PPI: The line plot shows the startle reactivity (in arbitrary units) obtained on pulse-alone and prepulse-plus-pulse trials averaged across all three pulse stimuli used. N = 14 in each experimental group; all values are means ± SEM.