Fig. 4
Tbr1+/− mice show AMPAR and NMDAR hypofunction at amygdalar thalamic-LA synapses, which are rescued by high dietary zinc. A Schematic of electrode placement in the LA for all electrophysiology experiments. LA: lateral amygdala; BA: basal amygdala. B Representative traces of half-maximal AMPAR-mediated EPSCs recorded from WT mice and heterozygous mutant Tbr1+/− mice fed with normal or high zinc diet. C Significantly reduced half-maximal amplitude of AMPAR-mediated EPSCs in Tbr1+/− thalamic-LA synapses are restored by high dietary zinc. (Sample size, neurons/animals: WT30ppm = 13/6, Tbr+/−30 ppm = 19/8, WT150ppm = 13/5, Tbr+/−150 ppm = 12/6). D Representative traces of AMPAR- and NMDAR-mediated EPSCs. E, F Tbr1+/− mice display significantly impaired NMDAR function, measured by both reduced average amplitudes of evoked NMDAR-mediated EPSCs and reduced NMDAR/AMPAR ratio, which is prevented by dietary zinc supplementation. E, F Sample size, neurons/animals: WT30ppm = 14/6, Tbr+/−30 ppm = 14/6, WT150ppm = 10/5, Tbr+/−150 ppm = 11/5). Each point represents data from individual neurons recorded in each experimental group. All data represent mean ± standard error of the mean, analysed using one-way analysis of variance with Tukey’s post hoc test. ns = not significant, *p < 0.05, **p < 0.01, ***p < 0.005, ****p < 0.001