Fig. 2

Impaired glutamatergic synaptic transmission of layer 2/3 pyramidal neurons in Shank3 mutant dogs. A The representative EPSCs and IPSCs of PFC pyramidal neurons from WT and Shank3 mutant dogs. EPSCs and IPSCs were evoked by 20%, 50%, and 100% saturation stimulus. B Comparison of EPSCs amplitude between WT and Shank3 mutant dogs (WT: n = 8 neurons, Shank3 mutant: n = 10 neurons; p = 0.0351, 0.7186, and 0.7889 for stimulus intensities at 20%, 50%, and 100% saturation levels, respectively). C Comparison of IPSCs amplitude between WT and Shank3 mutant dogs (WT: n = 8 neurons, Shank3 mutant: n = 11 neurons; p = 0.8698, 0.6016, and 0.7939 for stimulus intensities at 20%, 50%, and 100% saturation levels, respectively). D The normalized EPSCs and IPSCs in response to paired pulses with intervals of 50 ms and 200 ms. E Paired-pulse ratio of EPSCs of WT and Shank3 mutant dogs (WT: n = 14 neurons, Shank3 mutant: n = 12 neurons; p = 0.0003, 0.0236, 0.0648, and 0.0159 for paired-pulses intervals at 20 ms, 50 ms,100 ms, and 200 ms, respectively). F Paired-pulse ratio of IPSCs of WT and Shank3 mutant dogs (WT: n = 13 neurons, Shank3 mutant: n = 13 neurons; p = 0.6568, 0.6435, 0.6527, and 0.6097 for paired-pulses intervals at 20 ms, 50 ms,100 ms, and 200 ms, respectively). G Representative spontaneous EPSCs (sEPSCs) of PFC pyramidal neurons from WT and Shank3 mutant dog. H, J Cumulative distributions of amplitude and inter-events interval of sEPSCs (WT: n = 10 neurons, Shank3 mutant: n = 15 neurons; p < 0.0001). I, K The histograms for the amplitude (I) and frequency (K) of sEPSCs. Data in B, C, E, F, I and K were analyzed with a two-tailed, unpaired t test. Data in H and J were analyzed with Kolmogorov–Smirnov test. All data were collected from 3 pairs of animals, and presented as mean ± SEM; *p < 0.05, **p < 0.01 and ***p < 0.001