File:Lu Nicoll 2009 FIG5.jpg

Figure 5.

Deletion of GluA2A3, GluA1A3, or GluA1A2 in CA1 Pyramidal Cells (A) (A1–A5) Scatter plots (A1–A3) and bar graphs (A4 and A5) show amplitudes of EPSCs for single pairs (open circles) and mean ± SEM (filled circles) for GRIA2A3fl/fl (A1), GRIA1A3fl/fl (A2), and GRIA1A2fl/fl (A3), respectively. (A4) The amplitudes of AMPAR EPSCs were significantly reduced in all three cases (ΔGluA2A3, Cnt, −58.1 ± 11.4 pA; Cre, −24.9 ± 3.3 pA; n = 14; ∗p < 0.01; ΔGluA1A3, Cnt, −128.4 ± 19.7 pA; Cre, −15.6 ± 3.10 pA; n = 12; ∗p < 0.001; ΔGluA1A2, Cnt, −84.3 ± 10.1 pA; Cre, −4.9 ± 0.8 pA; n = 24; ∗p < 0.001). (A5) No change in the size of NMDAR EPSCs was observed (ΔGluA2A3, Cnt, 40.3 ± 7.4 pA; Cre, 38.0 ± 6.3 pA, n = 12; p = 0.82; ΔGluA1A3, Cnt, 49.2 ± 11.7 pA; Cre, 49.0 ± 13.7 pA, n = 11; p = 0.99; ΔGluA1A2; Cnt, 36.3 ± 5.8 pA; Cre, 31.0 ± 4.2 pA, n = 23; p = 0.31). (Inset in A1–A3) Sample traces are as follows: black, control; green, Cre. (B and C) Bar graphs show average RI (B) (Cnt, 0.99 ± 0.03, n = 30; ΔGluA2A3, 0.14 ± 0.02, n = 13; ∗p < 0.001; ΔGluA1A3, 1.06 ± 0.2, n = 5; p = 0.59; ΔGluA1A2, 0.1 ± 0.02, n = 6; ∗p < 0.001) and average PPR (C) (Cnt, n = 84; ΔGluA2A3, n = 14; ΔGluA1A3, n = 6; ΔGluA1A2, n = 11; p > 0.05 for each conditions). Left were sample traces. For GRIA1A2fl/fl cells, the stimulus was increased to record measurable EPSCs, and only recordings from the Cre cell were shown. (D) Sample recordings of mEPSCs at low gain and sweep speed (traces on left; scale bar, 10 pA, 500 ms) and averaged mEPSCs at high gain and sweep speed (traces on right). Control trace (black) has been superimposed on the trace from a Cre cell. Scale bar, 5 pA, 10 ms. (E) (E1) Bar graphs show mEPSC amplitude (top, Cnt, −10.51 ± 0.37 pA; ΔGluA2A3, −10.56 ± 0.60 pA; p = 0.93; ΔGluA1A3, −7.21 ± 0.36 pA; ∗p < 0.001; ΔGluA1A2, −6.79 ± 0.20 pA; ∗p < 0.001), (E2) frequency (middle, Cnt, 0.28 ± 0.03 Hz; ΔGluA2A3, 0.17 ± 0.05 Hz; ∗p < 0.005; ΔGluA1A3, 0.03 ± 0.01 Hz; ∗p < 0.001; ΔGluA1A2, 0.06 ± 0.01 Hz, ∗p < 0.001), and (E3) decay (bottom, Cnt, 11.30 ± 0.49 ms; ΔGluA2A3, 10.18 ± 1.2 ms; p = 0.33; ΔGluA1A3, 14.70 ± 0.71 ms; ∗p < 0.01; ΔGluA1A2, 4.20 ± 0.71 ms; ∗p < 0.001). n = 22, 14, 7, and 9 for Cnt, ΔGluA2A3, ΔGluA1A3, and ΔGluA1A2, respectively. (A–E) The recordings were made from acute hippocampal slices (P20–P27) from animals injected at P0–P1.