Fig. 1

Association of Jacob with the nuclear envelope requires activity of GluN2B but not GluN2A containing NMDAR. a, b Treatment of hippocampal primary neurons (DIV16/18) with the competitive NMDA receptor antagonist APV (20 µM) for 30 min in the presence of anisomycin results in decreased nuclear envelope association of Jacob. Scale bar indicates 10 µm. b Quantification of Jacob IR at the nuclear rim. (***) indicate p < 0.001 (ANOVA, Bonferroni). c, d Chronic treatment of neurons with ifenprodil (5 µM) but not with NVP-AAM077 (50 nM) abolished Jacob nuclear IR as well as association with the nuclear envelope. Depicted are confocal images of hippocampal primary neuron at DIV16/18 immunolabeled with anti-Jacob antibody and co-labeled against MAP2 and stained with DAPI. d Quantification of Jacob IR in the nucleus upon the treatment. (***) indicate p < 0.001; n.s. = non-significant (ANOVA, Bonferroni). e, f Treatment of hippocampal primary neurons (DIV16/18) with ifenprodil (5 µM) for 30 min during enhanced synaptic activity prevents accumulation of Jacob at the nuclear envelope. Scale bar indicates 10 µm. b Quantification of Jacob IR at the nuclear rim. (***) indicate p < 0.001 (Two-tailed t-test)