Figure 7.

Loss of ClC-2 in interneurons leads to an increased inhibition. A, ClC-2 is expressed in a subset of interneurons. Sample trace of a ClC-2 current from an interneuron identified by biocytin filling. B, C, Evoked IPSCs were measured as a function of the stimulus strength in CA1 pyramidal cells in response to extracellular stimulation by a microelectrode positioned nearby. Sample traces for WT (left) and KO (right) (B). Averaged data reveal an increase of IPSCs (C). D, Paired-pulse ratio, a measure for presynaptic release, shows no difference between WT and KO. Sample traces on the left. Stimulus artifacts have been omitted for clarity. E, Sample traces of sIPSC recordings for WT (left) and KO (right). F, Cumulative frequency distribution of sIPSC amplitudes (p < 0.001, Kolmogorov–Smirnov test; n = 24 for WT; n = 24 for KO). Inset shows mean amplitude. G, Cumulative frequency distribution of sIPSC frequencies (p = 1, Kolmogorov–Smirnov test; n = 18 for WT; n = 18 for KO). Inset shows mean frequency. H, Sample traces for mIPSC recordings for WT (left) and KO (right). I, Cumulative frequency distribution of mIPSC amplitudes (p = 1, Kolmogorov–Smirnov test; n = 22 for WT; n = 23 for KO). Inset shows mean amplitude. J, Cumulative frequency distribution of mIPSC frequencies (p = 1, Kolmogorov–Smirnov test; n = 22 for WT; n = 23 for KO). Inset shows mean frequency. Error bars represent SEM in all graphs.