Local regulation of dendritic GluA1 by miR-501-3p. In A and B, primary neurons were treated with NMDA (30 µM for 5 min) and collected at 90 min after treatment to test for miR-501-3p. (A) The level of miR-501-3p in whole cell lysates; n = 3–5 experiments. (B) miR-501-3p associated with RISC; n = 3–4 experiments. In C and D, transfected hippocampal neurons (17 DIV; 3 d after transfection) were treated with NMDA, and then stained for GluA1. (C) Representative images of transfected neurons. (D) Quantification of C; n = 14–29 cells for each group; AP5 was added 10 min before treatment and present during and after NMDA treatment. In E–G, hippocampal slices in which cell bodies of CA1 pyramidal neurons were removed or intact hippocampal slices were treated with NMDA (30 µM for 5 min). (E) Representative immunoblots. (F) Quantification of E; n = 4 rats for the intact slice group and 6 rats for the neuropil group. (G) miR-501-3p expression normalized to U6; n = 5 rats for the intact slice group and 6 rats for the neuropil group. Data are presented as mean ± SEM; Mann-Whitney U test is used for statistical analysis; *, P < 0.05; **, P < 0.01; ***, P < 0.005. Bar, 5 µm.