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. Author manuscript; available in PMC: 2012 Jul 13.
Published in final edited form as: Development. 2007 Nov;134(22):4083–4093. doi: 10.1242/dev.008524

Fig. 3. Consequences of PV-interneuron loss in cD2−/− brain.

Fig. 3

(A–C) Whole-cell voltage-clamp recordings in acute slices show GABAA receptor-mediated miniature inhibitory postsynaptic currents (mIPSCs) in frontal cortical pyramidal neurons. (A) Example traces under conditions isolating GABAA receptor-mediated mIPSCs (see text). (B) Mean frequency distribution of mIPSC amplitudes in cD2 mutant (black) and WT (gray) neurons. (C) Average frequency of mIPSCs of all amplitudes. *, cD2 nulls<WT, P<0.05. (D–F) Cortical electroencephalographic (EEG) recorded by telemetry from awake-behaving mice. (D) Example traces for cyclin cD2−/− and WT siblings show intermittent bursts of faster frequency discharges in the cD2 null. (E) Mean normalized power spectral density (nPSD) distribution over 1000 seconds, collected in randomly selected blocks of 10 seconds each in cD2 mutant (black) and WT (gray) with 25 Hz bin resolution. (F) Average of mean nPSD of EEG for low (1–175 Hz) and high (200–375 Hz) frequency. *, P<0.05, as compared with WT.