Fig. 1

Higher visual areas in Angelman syndrome model mice show stimulus-specific deficits in activity modulation. a Schematic of intrinsic signal optical imaging (ISOI) used to identify the boundaries and measure activity in HVAs. Visual stimuli were presented to the contralateral (left) eye to a lightly anesthetized mouse via an LCD screen. Magnitude and phase maps in response to multiple stimuli were obtained. Phase maps evoked by a single drifting bar stimulus were used to determine retinotopy. b Representative magnitude maps of primary and higher visual areas of WT and AS model mice in response to still-fast (0➔50°/s) and slow-fast (10➔50°/s) gratings. ΔR/R, normalized to V1. White lines designate boundaries between visual areas determined by retinotopy; solid lines indicate regions quantified in (c); dashed lines indicate regions not quantified. Scale bar, 1 mm. c Quantification of the amplitude of responses of HVAs LM, AL, and RL to still-fast and slow-fast gratings, normalized to V1 activation for each stimulus. Each animal’s response to both stimuli is connected by a line. Two-tailed paired t test. *p < 0.05; **p < 0.01; ***p < 0.001. d Stimulus-response curves in HVAs LM, AL, and RL to stimuli in which only the starting speed is changed. LM: stimulus effect (p = 0.0001), genotype effect (p = 0.0002), and interaction effect (p = 0.0211). AL: stimulus effect (p < 0.0001), Genotype effect (p < 0.0001), and interaction effect (p = 0.007). RL: stimulus effect (p < 0.0001), genotype effect (p = 0.0003), and interaction effect (p = 0.0008). Two-way ANOVA. Tukey’s post hoc. ****p < 0.0001