Figure 9.

NMDAR activation induces a long-lasting decrease in synaptic AMPAR number. a–d, Representative images showing surface GluR2 (red) and synapsin-1 (green) protein immunolabeling in neurons at 4 h after treatment with vehicle(a), NMDA (b), actinomycin D (c), and NMDA (d) in the presence of actinomycin D. e, Time course of surface and total GluR2 protein in dendrites after treatment with NMDA. f, Quantitative analysis of total GluR2 protein abundance in dendrites at 4 h after NMDA, actinomycin D, NMDA plus actinomycin D, emetine, and NMDA plus emetine. g, Quantitative analysis of synaptic GluR2 assessed in images like those in a–d. NMDAR stimulation (30 s) markedly reduced surface and total GluR2 protein abundance in dendrites, with little or no change in soma (b, e, f). NMDA did not detectably alter NR1 protein fluorescence in dendrites (data not shown). Emetine and actinomycin D mimicked and occluded the NMDA-induced loss of GluR2 protein in dendrites (f) and synaptic sites (g). Drug treatments were as described in Materials and Methods. Data represent the percentage change in the mean integrated intensity values per designated area of interest for a minimum of four independent experiments. Error bars represent SEMs (**p ≤ 0.01). Scale bars: a–d, 10 μm; insets, 2 μm.