Chunk #1 — Figure 2

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PDZ binding of TARPγ-8 controls synaptic transmission but not synaptic plasticity.

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The ©-8 PDZ ligand modulates AMPAR-mediated basal transmission, but not LTP. (a) Ratio of AMPAR- to NMDAR-EPSCs is reduced by ~30% in CA1 pyramidal cells from γ-8Δ4/Δ4 slices (n=11) compared with those from γ-8+/+ slices (n=5). Representative examples of averaged EPSCs (AMPAR current=light trace; NMDAR current=dark trace). Calibration: 100 ms, 20 pA (+/+) and 16 pA (⊗4/⊗4). (b) Ratio of stimulus intensity (input) to the EPSP slope (output). Input-output was significantly reduced in slices from γ-8Δ4/Δ4 (n=6) compared to those from γ-8+/+ mice (n=10). * P < 0.05 paired t-test. (c) 100 nM AMPA-evoked whole cell currents are reduced by ~38% in γ-8Δ4/Δ4 (n=8) compared to γ-8+/+ mice (n=7). Inset, AMPA-evoked current from representative cells are shown. Calibration: 1 min, 50 pA. (d) Extracellular recordings of field EPSPs before and after tetanic stimulation of Schaffer collaterals (arrow). LTP was elicited in γ-8+/+ (open squares; n=6), γ-8Δ4/Δ4 (gray squares; n=10) and γ-8+/Δ4 slices (light gray squares; n=9) to a similar degree, but attenuated in γ-8−/−slices (black triangles; n=4). Inset, averaged fEPSPs before (dark trace) and during LTP (light trace). Calibration: 10 ms, 0.5 mV (+/+), 0.45 mV (⊗4/⊗4), 0.38 (+/⊗4) and 0.5 mV (−/−). (e) Whole-cell recordings from CA1 pyramidal cells before and after a pairing protocol (arrow). LTP was induced in slices from γ-8+/+ (n=5), γ-8+/Δ4 heterozygote (n=4) and γ-8Δ4/Δ4 homozygote mice (n=6). Inset, representative examples of averaged EPSCs recorded before and during LTP. Calibration: 20 ms, 200 pA (+/+), 160 pA (⊗4/ ⊗4) and 200 pA (+/⊗4). All data are given as mean ± s.e.m.; * P < 0.05.