We also found evidence for increased expression of GABAergic phenotypes electrophysiologically. Although the size of sodium currents in control- and proband-derived neurons was similar (Figure S3), there was substantial cell-to-cell variation in the voltage dependence of activation and inactivation, suggesting that different neurons express different proportions of brain sodium channel isoforms (Nav1.1, Nav1.2, Nav1.3, Nav1.6). Figure 5 shows results for steady-state inactivation. Neurons from probands and their familial controls displayed substantial variation in the pre-test potential (Vpre) at which the peak sodium current was reduced to half its maximal amplitude (Eh1/2), and adequate fits to some of the data required two Hodgkin-Huxley components (Figure 5D, E). Interestingly, sodium currents in proband-derived neurons tended to inactivate at more hyperpolarized membrane potentials than the corresponding currents in control neurons (Figure 5C–E; n=7 ASD and 10 control neurons). The increased proportion of proband-derived neurons that gave Eh1/2 values in the range −72 to −65 mV (Figure 5F) is consistent with increased expression of the Nav1.1 isoform in these cells. This isoform is preferentially expressed in GABAergic interneurons (Cheah et al., 2012; Han et
