Fig. 4
Maternal zinc supplementation does not alter cortico-striatal glutamatergic synapse function in three-week-old Shank3−/− offspring mice. MSN striatal evoked AMPAR- and NMDAR-mediated EPSC amplitudes measured in 3 week old wildtype (WT) and Shank3−/− offspring mice from normal and supplemented maternal zinc diet groups. a No significant differences were observed in AMPAR EPSC amplitudes between WT or Shank3−/− offspring mice from either maternal zinc diet group (WT control maternal zinc diet (MZD) n = 13 neurons from 3 mice, Shank3−/− control MZD n = 14 neurons from 4 mice, WT supplemented MZD n = 10 neurons from 2 mice, Shank3−/− supplemented MZD n = 10 neurons from 2 mice). b No significant differences were observed in paired-pulse ratio between either genotypes or maternal dietary zinc groups (WT control MZD n = 9 neurons from 3 mice, Shank3−/− control MZD n = 11 neurons from 4 mice, WT supplemented MZD n = 10 neurons from 2 mice, Shank3−/− supplemented MZD n = 8 neurons from 2 mice). c Evoked NMDAR-mediated EPSC amplitudes in WT and Shank3−/− offspring mice from either maternal zinc group were not significantly different (WT control MZD n = 8 neurons from 3 mice, Shank3−/− control MZD n = 8 neurons from 4 mice, WT supplemented MZD n = 5 neurons from 2 mice, Shank3−/− supplemented MZD n = 7 neurons from 2 mice). d Decay kinetics, measured as the weighted time constant tau (tw), were also not significantly different across experimental groups (WT control MZD n = 6 neurons from 3 mice, Shank3−/− control MZD n = 7 neurons from 4 mice, WT supplemented MZD n = 5 neurons from 2 mice, Shank3−/− supplemented MZD n = 7 neurons from 2 mice). All values are presented as mean ± standard error of the mean. Individual data points represent individual neurons, and were statistically analysed using two-way ANOVA with Tukey’s multiple comparisons test. NS = not significant