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. 2015 Oct 28;112(45):14072–14077. doi: 10.1073/pnas.1518773112

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Fig. 4. — Deactivation of L1 INs in silico predicts increase of L2 PSP variability. (A) The same model configuration as in Fig. 3, but without L1 INs in the PC. (B) Comparison of whisker-evoked PSP variability between models with (Left) and without (Right) PC L1 INs (each gray line refers to one of the 50 anatomical models). (C) Sensitivity analyses from left to right: varying functional connectivity of PN synaptic contacts; keeping PN functional connectivity fixed and deactivating PC L1 INs; removing NMDARs from PN synapses; varying L1 IN synapse strengths around the value used in all simulations (1.6 nS). (D) L1 IN inputs shunt dendritic branches as quantified by the shunt level (SL). The average (across trials) SL decreases monotonically toward proximal dendrites, reaching zero ∼100 µm from the soma. (E) Change (with vs. without L1 INs) of the average (across trials) membrane potential (ΔV_m) and its variability (ΔSD), calculated at multiple dendritic locations in the presence (Upper) and absence (Lower) of NMDARs in the model.