Fig. 5

Blocking Autophagic Flux Increases Tau Secretion and Occludes the Effects of p300 a Schematic diagram showing autophagic flux and predicted changes in autophagic markers with baflomycin A1 (BafA1) treatment. b–f BafA1 treatment in primary neurons. b Representative immunoblots of LC3-I, LC3-II, p62 and actin in lysates of rat primary neurons treated with BafA1 (10 nM) or control (ctrl, DMSO) for 24 h. Quantification of levels of LC3-II (c) and p62 (d) relative to actin, normalized to control. e Quantification of intracellular tau levels by ELISA, normalized to control. f Quantification of tau secretion over 3 h by ELISA, normalized to intracellular tau levels and normalized to control. (b–f) n = 6 wells from three independent experiments. ***p < 0.001, **p < 0.01, *p < 0.05 by unpaired t test. g Quantification of tau secretion over 3 h in primary neurons treated with BafA1 (10 nM), CTB (50 μM) or combined, normalized to intracellular tau levels and normalized to control (CTB- BafA1-). n = 6 wells from three independent experiments. **p < 0.01, *p < 0.05, ns, non-significant by one-way ANOVA and Sidak’s multiple comparisons test. h Quantification of tau secretion over 3 h in neurons treated with BafA1 (10 nM), 37892 (50 μM) or combined, normalized to intracellular tau levels and normalized to control (37892- BafA1-). n = 6 wells from three independent experiments. *, #p < 0.05, ***p < 0.001 by one-way ANOVA and Sidak’s multiple comparisons test. Values are mean ± SEM