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Fig. 2 | Molecular Neurodegeneration

Fig. 2

From: Phosphorylation of tau at Y18, but not tau-fyn binding, is required for tau to modulate NMDA receptor-dependent excitotoxicity in primary neuronal culture

Fig. 2

Tau modulates glutamate-induced excitotoxicity in cultured neurons. Glutamate-induced neurotoxicity in neuronal cultures from WT or tau-deficient (Mapt −/−) mice was assessed as in Fig. 1. Some cultures were transduced with lentiviral vectors encoding shRNA against tau (shTau) or scrambled shRNA (shSCR) at the day of plating or with lentiviral vectors encoding GFP-P2A-mTauWT or GFP-P2A at DIV7, as indicated. a, b Expression of shTau improved survival in WT a but not Mapt −/− b cultures. c Relative tau levels in WT and Mapt −/− cultures expressing shSCR or shTau were determined by western blot analysis with the pan-tau antibody EP2456Y and densitometric analysis of tau signals. Mean tau levels in shSCR-expressing WT cultures were arbitrarily defined as 1.0. d, e Overexpression of mTauWT increased glutamate-induced neurotoxicity (i.e., decreased survival) in WT d and Mapt −/− e cultures. f Relative tau levels in WT and Mapt −/− cultures expressing GFP-P2A or GFP-P2A-mTauWT were determined as in c. Mean tau levels in GFP-P2A-expressing WT cultures were arbitrarily defined as 1.0. Numbers of independent experiments (n) with cumulative well numbers per condition in parentheses: a 7 (42–56), b 4 (21–32), c 4–7 (1), d 4 (30–32), e 15 (106–120), and f 4–15 (1). When comparing mean differences across all doses within any given panel, a one-sided, one-sample t-test revealed significant differences between experimental and control conditions in (a, P < 0.01) and (e, P < 0.0001). **P < 0.01, ***P < 0.001, ****P < 0.0001 vs. control within same genotype by two-way ANOVA and Tukey test. Boxplots were explained in Fig. 1. Data in c, f are means ± SEM

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