Fig. 6: Grin2a was upregulated in the hippocampus of Mir125b-2^m−/p− mice.

a Venn diagram showing the overlap among four databases from RNA-Seq from Mir125b-2^m−/p+ mice and three software programs (miRDB, microT-CDS, and TargetScan) for predicting targets of Mir125b-2. b Gene ontology (GO) analysis of Mir125b-2 target genes. c Mir125b-2 target site on the 3′ untranslated region (3′UTR) of Grin2a²¹. d Levels of Grin2a in Mir125b-2^m−/p− mice and corresponding wild-type (Mir125b-2^m+/p+) controls. Mann–Whitney rank-sum test. Mir125b-2^m+/p+, n = 6 mice. Mir125b-2^m−/p−, n = 6 mice. e The luciferase assay for Grin2a 3′UTR with and without the miR-125b-2 binding site. The luminescence ratio was calculated as the firefly luciferase signal/Renilla luciferase signal for each well. The Grin2a_mut construct was derived from Grin2a 3′UTR with the deletion of the miR-125b-2 binding site. f Levels of Grin2a during brain development from postnatal day 0 (P0) to P28. One-way ANOVA with Fisher LSD Method post hoc comparison. n = 3/group. *P < 0.05, **P < 0.01, *P < 0.001. g Schematic of cell patching on hippocampal granule cells (GC) at postnatal day 28 (P28) for measurements of evoked excitatory postsynaptic currents. h Representative traces of AMPAR-mediated currents (AMPAR-EPSC) and NMDAR-mediated currents (AMDAR-EPSC) recordings from granule cells of Mir125b-2^m+/p+ (upper, black) and Mir125b-2^m−/p− (lower, green) mice. Scale bar represents 15 pA and 25 ms. i Both AMPAR- and NMDAR-mediated currents increased in Mir125b-2^m−/p− (green) mice compared with Mir125b-2^m+/p+ (black) mice. j the ratio of amplitudes from AMPAR-mediated and NMDAR-mediated currents did not differ between Mir125b-2^m+/p+ (black) and Mir125b-2^m−/p− (green) mice. Nine cells from three Mir125b-2^m+/p+ mice; 10 cells from three Mir125b-2^m−/p− mice. Student’s t-test, two-tailed, *P < 0.05, ***P < 0.01. All data are the mean ± s.e.m.