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Fig. 2 | Molecular Autism

Fig. 2

From: Dietary zinc supplementation rescues fear-based learning and synaptic function in the Tbr1+/− mouse model of autism spectrum disorders

Fig. 2

High dietary zinc rescues social interaction deficits in Tbr1+/− mice. A Heat maps representing example movements of animals during the social interaction test. B Both WTmice and heterozygous mutant Tbr1+/− mice spend significantly more time closely interacting with stranger 1 mouse (S1) than with the empty cup in the empty chamber (Empty: E), whether fed with the normal zinc diet (30 parts per million) or the high zinc diet. C Tbr1+/− mice fed the normal zinc diet show a significant deficit in preference index (measured as the difference in time spent between S1 and Empty). The preference index is restored to that of WT mice when the Tbr1+/− mice are fed with the high zinc diet. D Heat maps representing the example movements of animals during the social novelty test. E Dietary zinc supplementation did not rescue social novelty recognition deficit in Tbr1+/− mice, measured by the time spent in closely interacting with familiar stranger 1 (S1) mice or novel stranger 2 (S2) mice. F The social preference index derived from these results, is not different between WT mice and Tbr1+/− mice and this is not changed by dietary zinc supplementation. Each point represents individual mice in each experimental group (Sample size: WT30ppm = 11, Tbr+/−30 ppm = 11, WT150ppm = 9, Tbr+/−150 ppm = 11). All data represent mean ± standard error of the mean, analysed using two-way analysis of variance (ANOVA) with Šídák's post hoc test and one-way ANOVA with Tukey’s post hoc test. ns = not significant, *p < 0.05, **p < 0.01, ***p < 0.005, ****p < 0.001

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