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. 2021 Oct 8;29(3):657–669. doi: 10.1038/s41418-021-00881-1

Fig. 1. Nlrp1, Casp1, or Casp6 genetic ablation prevents cognitive deficits in J20 mice.

Fig. 1

A Distance traveled in open field task [F = 8.921, p < 0.0001, n = 18 WT, 15 J20, 10 J20/Nlrp1−/−, 13 J20/Casp1−/−, 10 J20/Casp6−/−, 13 WT/Nlrp1−/−, 12 WT/Casp1−/−, 12 WT/Casp6−/−, 14 J20/Nlrp1+/−, 12 J20/Casp1+/−, 11 J20/Casp6+/−, 12 WT/Nlrp1+/−, 13 WT/Casp1+/−, 11 WT/Casp6+/−]. B NOR DI [F = 8.081, p < 0.0001, n = 16 WT, 15 J20, 10 J20/Nlrp1−/−, 13 J20/Casp1−/−, 11 J20/Casp6−/−, 13 WT/Nlrp1−/−, 12 WT/Casp1−/−, 12 WT/Casp6−/−, 14 J20/Nlrp1+/−, 11 J20/Casp1+/−, 11 J20/Casp6+/−, 12 WT/Nlrp1+/−, 13 WT/Casp1+/−, 11 WT/Casp6+/−]. C Barnes maze learning acquisition showing primary errors (top) and primary latency (bottom) to reach target of +/− (right) and −/− (left) mice [Primary errors performance: Ftraining day = 142.5, p < 0.0001, Fgenotype = 4.455, p < 0.0001, 2-way ANOVA, n = 16 WT, 13 J20, 10 J20/Nlrp1−/−, 13 J20/Casp1−/−, 9 J20/Casp6−/−, 13 WT/Nlrp1−/−, 12 WT/Casp1−/−, 12 WT/Casp6−/−, 12 J20/Nlrp1+/−, 11 J20/Casp1+/−, 10 J20/Casp6+/−, 11 WT/Nlrp1+/−, 12 WT/Casp1+/−, 10 WT/Casp6+/−]. D Barnes maze probe showing primary errors (top) and primary latency (bottom) to blocked target [F = 1.915, p = 0.0324, n as in C]. E–H Golgi–Cox quantification (n = 15 WT, 10 J20, 6 J20/Nlrp1−/−, 7 J20/Casp1−/−, 5 J20/Casp6−/−) E Dendritic spine density, and the % of F mushroom, G thin, and H stubby dendritic spines, in hippocampal CA1 SR. Synaptophysin quantification (n = 9 WT, 9 J20, 5 J20/Nlrp1−/−, 6 J20/Casp1−/−, 4 J20/Casp6−/−) in hippocampal I DG [F = 12.10, p < 0.0001], J CA3 stratum lucidum (SLu) [F = 9.731, p < 0.0001], and K CA1 SR. Bars represent mean ± SEM of all mice per group; symbols denote performances of individual mice. For A, B, D–K, one-way ANOVA, Bonferroni’s post-hoc compared to WT (#) or J20 (*). # or *p < 0.05, ## or **p < 0.01, ### or ***p < 0.001, #### or ****p < 0.0001.