Fig. 6: Enhanced EAAT2 expression underlies impaired astrocyte activity and memory in astrocytic NLG3 KO mice.
a, b Increased GCaMP6f fluorescence in both GFAP-NLG3 WT (n = 26 cells, 3 mice, p = 0.00000169) and KO (n = 26 cells, 3 mice, p = 0.00198) astrocytes after (post) glutamate treatment compared to before (pre). c Activated astrocytes in GFAP-NLG3 WT (n = 6 slices from 3 mice) and KO (n = 6 slices from 3 mice) slices treated with glutamate. d, e Increased GCaMP6f signals in response to HFS in GFAP-NLG3 WT (n = 24 cells, 3 mice, p = 0.00540) and KO (n = 24 cells, 3 mice, p = 0.00000000212) astrocytes treated with TBOA, but not in GFAP-NLG3 KO astrocytes treated with ACSF (n = 28 cells, 4 mice). f Activated astrocytes in TFB-TBOA treated GFAP-NLG3 KO (n = 6 slices, 3 mice, p < 0.001) and WT slices (n = 5 slices, 3 mice), compared to ACSF treated GFAP-NLG3 KO (n = 6 slices, 3 mice), g Local TFB-TBOA injections to ventral hippocampus before behavior tests. h GFAP-NLG3 KO mice treated with saline (n = 8 mice, p < 0.001) or TFB-TBOA (n = 8 mice, p < 0.001) preferred S1 over E during Stage 2 of three-chamber test. i GFAP-NLG3 KO mice treated with TFB-TBOA (n = 8 mice), but not with saline (n = 8 mice), preferred S2 over S1 during Stage 3 of three-chamber test (sniffing time p < 0.001, memory index p < 0.001). Data represent mean ± SEM; two-tailed paired t test for (b and e); two-tailed t test for (c) and right panel of (i); one-way ANOVA test with Holm-Sidak test for (f); two-way ANOVA with Tukey post hoc multiple comparisons for (h) and left panel of (i); **p < 0.01, ***p < 0.001. Scale bar: 0.5 dF/F0 /5 s in (a and d). Source data are provided as a Source Data file.
