Fig. 3: FORTIS can detect decreases in surface GluA1 following cLTD induction.

a An immunoblot showing the levels of Ser 845 phosphorylated GluA1 or total GluA1 20 min after a 5-min exposure to different NMDA concentrations. Lower panel, in some cultures cLTD (20 μM NMDA) was induced in the presence of the NMDA inhibitor APV (50 μM). b, c Quantification of Ser 845 phospho-GluA1 following NMDA treatment with or without the inhibitor APV (50 μM). N represents the number of cultures, and the p value was determined with one-way ANOVA followed by Dunn’s multiple comparison tests. d, e Changes in endogenous and recombinant (SEP-GluA1 or pHuji-GluA1) Ser 845 GluA1 phosphorylation (normalized to vehicle) following treatment with NMDA (50 μM). N represents the number of cultures, and the p values were determined by one-way ANOVA followed by Holm–Sidak’s multiple comparisons test. f Heat map of the changes in SEP-GluA1 fluorescence (ΔF/F₀, %) where each square represents a single cortical culture in a 96-well plate 120 min after a 5-min exposure to two concentrations of NMDA, as indicated. g Changes in SEP-GluA1 fluorescence when two NMDA concentrations were used to induce cLTD. Fluorescence was measured 30 and 120 min after 5-min treatment with NMDA. N represents the number of cultures, and the p values were determined by Dunnett’s multiple comparison test, representing the data as the mean ± SEM.