Figure 4
NR2B-containing NMDAR inhibition but not NR2A-containing NMDAR knockout abolishes hTau-dependent toxicity after activation of extrasynaptic NMDARs. (a) Representative confocal images of primary neurons expressing EGFP-hTau after extrasynaptic activation in the presence and absence of 3 μM Ifenprodil. (b) Representative confocal images of primary neurons from NR2AKO mice expressing EGFP-hTau after extrasynaptic activation. (c) Confocal images of EGFP-hTau-expressing primary neurons from NR2AKO mice after extrasynaptic activation and immunostaining against βIII tubulin. (d) Quantification of hTau-dependent toxicity in the presence and absence of Ifenprodil. Shown is the ratio of non-degenerated infected neurons (neurons without fragmented or beaded neurites or ballooned morphology) to total infected neurons. (e) Quantification of hTau-dependent toxicity in primary neurons of NR2AKO mice. eSyn act, activated eSyn NMDARs; values are shown as mean±S.E.M. with ***P<0.001; Mann–Whitney-U-test; n=10–14; scale bar: 50 μm
