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. 2021 Jun 28;15:676891. doi: 10.3389/fncir.2021.676891

Figure 2.

Figure 2

The NLGN3-R451C mutation impairs CF synapse elimination during postnatal development. (A–E) Specimen records of CF-EPSCs (inserts, five to eight traces were superimposed at each threshold intensity; Vh = −10 mV) and frequency distribution histogram for the number of discrete CF-EPSCs for wild-type (open columns) and NLGN3-R451C mutant mice (orange columns) at indicated ages. There is no significant difference in the frequency distribution in (A,B,E) between wild-type and NLGN3-R451C mutant mice [(A), p = 0.143, (B), p = 0.063, and (E), p = 0.6 by Mann-Whitney U test]. In contrast, frequency distributions for (C,D) are significantly different between wild-type and NLGN3-R451C mutant mice (C, *p = 0.024 and D, **p < 0.001 by Mann-Whitney U test). Scale bars, 10 ms and 0.5 nA. Numbers of PCs/mice are shown in parentheses. (F) Summary plots of disparity ratio in wild-type (open circles) and NLGN3-R451C mutant (orange circles) mice at indicated ages. There is a significant difference between wild-type and NLGN3-R451C mutant mice aged P16–P20 (P5–P6, p = 0.961; P7–P9, p = 0.877; P10–P12, p = 0.409; P13–P15, p = 0.173; P16–P20; *p = 0.039 by Two-way ANOVA with Tukey's post-hoc test). Numbers of PCs/mice are shown in parentheses. Data are expressed as mean ± SD.