NKCC1 blockade plus BUM treatment alleviates aberrant neuronal excitability in developing Ecm29 KO neurons. (A1) Representative differential interference contrast (DIC) images of whole-cell patch clamp recordings of layer V pyramidal neurons in mPFC slices prepared from P7–P9 mice. ACd, dorsal anterior cingulated cortex; IL, infralimbic cortex; PL, prelimbic cortex. (A2) Graphs summarizing various intrinsic membrane properties of mPFC layer V neurons in wild-type (Ecm29^+/+) and Ecm29 KO (Ecm29^−/−) mice in the presence or absence of the NKCC1 inhibitor BUM (10 µM; ±SEM, n > 20 per group; *, P < 0.05; **, P < 0.01; ns, not significant by unpaired t test or two-way ANOVA followed by Tukey's multiple comparison test). C_m, membrane capacitance; R_in, input resistance. (B1) Representative traces of APs evoked by a 40-nA step current with or without 10 µM BUM application. (B2) Graphs show that mPFC layer V neurons of Ecm29 KO (Ecm29^−/−) mice exhibit hyperexcitability (as reflected by spike probability, number, and frequency) at different current steps, and that hyperexcitability is abolished by BUM application. Data (±SEM, n > 20 per group) obtained from the same sets of experiments shown in A2. *, P < 0.05 compared with wild-type group by multiple t tests.