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. Author manuscript; available in PMC: 2017 Dec 21.
Published in final edited form as: Neuron. 2016 Dec 8;92(6):1337–1351. doi: 10.1016/j.neuron.2016.11.017

Figure 6. MiR-101 targets NKCC1, Kif1a, and Ank2 to restrain synaptic events and balance E/I.

Figure 6

(A) Recording sEPSCs in P11 acute hippocampal slices from control (a-Ctrl) and a-101.F-treated mice. The a-101.F treatment increased the frequency of sEPSCs (B) but not sIPSCs (C), and therefore increased the ratio of sEPSCs/sIPSCs (D). (E) Traces of mEPSCs (at −80 mV) and mIPSCs (at 0 mV) from a-Ctrl- (top, left), a-101.F-treated (bottom, left), NKCC1-TSB-treated (top, right), and G1-treated (bottom, right) animals. Both mEPSC (F) and mIPSC (G) frequencies were increased (see also Figure S9D), though mEPSCs proportionately more so by a-101.F, causing an increased mEPSC/mIPSC (H). G1 treatment better replicated a-101.F than did NKCC1-TSB (F, H), indicating the additive effects of multiple pathways. Bar graphs: mean ± s.e.m. One-way ANOVA with Tukey’s multiple comparison test (B–D), Kruskal Wallis with Dunn’s multiple comparison test (F–H). *p<0.05; **p<0.01; ***p<0.001.