Supplementary Figure 2: Comparison of Nrxn3α/β cKO and Nrxn3α KO on synaptic properties of cultured hippocampal neurons.
a. Conditional Nrxn3α/β KO does not alter passive membrane properties (left, input resistance; right, membrane capacitance). Hippocampal neurons were cultured from newborn homozygous Nrxn3α/β cKO mice, infected with inactive (control) or active cre-recombinase (cre) at DIV2-4, and analyzed on DIV14-16 (Rm: p = 0.612; Cm: p = 0.646).
b & c. mEPSC and mIPSC kinetics are not changed by the conditional Nrxn3α/β KO. Representative traces (top) and summary graphs (bottom) of mEPSC (b; rise: p = 0.995; decay: p = 0.861) and mIPSC (c; mIPSCs: rise: p = 0.876; decay: p = 0.800) rise and decay kinetics, measured in neurons obtained as in (a).
d. The Nrxn3α/β cKO does not decrease the release probability at excitatory synapses, measured using the stimulus-dependent NMDAR blockade by MK-801 during low-frequency stimulation. Neurons were obtained as described in a (p = 0.710).
e. Constitutive Nrxn3α KO does not alter passive membrane properties (left, input resistance; right, membrane capacitance). (Rm: p = 0.569; Cm: p = 0.670).
f. Constitutive Nrxn3α KO does not alter spontaneous mEPSCs (left, representative traces; right, summary graphs of the mEPSC frequency (p = 0.0676) and amplitude (p = 0.613)..
g-i. Constitutive Nrxn3α KO does not alter evoked AMPAR-mediated (g; p = 0.842) or NMDAR-mediated EPSCs (h; p = 0.767) or the PPR of NMDAR-mediated EPSCs (i; 100ms ISI: p = 0.553). For each panel, representative traces are shown on the left and summary graphs on the right..
Data shown represent means ± SEM of individual experiments; number of cells patched/experiment analyzed are shown in the bars or plots. For (i), mean ± SEM was calculated from number of cells. Statistical significance was assessed by single-factor ANOVA.
