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Corrigendum for Riekki et al., J Neurophysiol 99 (6) 3075-3089.
J Neurophysiol 100: 1691-1694, 2008; doi:10.1152/jn.z9k-9011-corr.2008
0022-3077/08 $8.00
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CORRIGENDUM

Corrigendum

Volume 99, June 2008Riekki R, Pavlov I, Tornberg J, Lauri SE, Airaksinen MS, Taira T. Altered Synaptic Dynamics and Hippocampal Excitability but Normal Long-Term Plasticity in Mice Lacking Hyperpolarizing GABAA Receptor-Mediated Inhibition in CA1 Pyramidal Neurons. J Neurophysiol 99: 3075–3089, 2008. First published April 24, 2008; doi:10.1152/jn.00606.2007; http://jn.physiology.org/cgi/content/full/99/6/3075.

During production, Figs. 1, 2, 3, and 6, were misrepresented. The correct versions appear below.


Figure 1
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FIG. 1. Reversal potentials of GABAA receptor (GABA-AR)-mediated currents in CA1 pyramidal neurons in wild-type (WT) and KCC2-deficient mice (KCC2hy/null) mice. A: sample current traces taken at –90 to –20 mV; left, WT; right, KCC2hy/null. B, left: average GABAA reversal potentials in WT (n = 5 cells/5 animals) and KCC2hy/null mice (n = 6/4). Individual experiments marked (bullet, {circ}). Right: I-V plots for the GABA-R-mediated currents. **, P < 0.01.

 

Figure 2
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FIG. 2. Basic properties of field inhibitory postsynaptic potentials (fEPSPs) in the CA1 stratum radiatum in WT and KCC2hy/null mice. A: example traces and pooled data to illustrate fEPSPs evoked by single pulse stimulation of increasing intensity. No significant differences between the genotypes were observed (WT, n = 8/3; KCC2hy/null, n = 10/4). B: analysis of the paired-pulse ratio at different interpulse intervals at the 2 genotypes. Pooled data and example traces illustrate significantly higher paired-pulse facilitation in the KCC2hy/null mice at long intervals as compared with the WT's (WT, n = 9/4; KCC2hy/null, n = 16/6; * = P < 0.05).

 

Figure 3
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FIG. 3. Analysis of fEPSPs during repetitious stimulations in WT and KCC2hy/null mice. At each frequency, significant (P < 0.05) augmentation of fEPSP's during repeated stimulation. A: analysis of fEPSP slope during the train of 100 pulses at 1 Hz (WT, n = 6/5; KCC2hy/null, n = 7/6). Example traces represent average of the 3 1st and 3 last fEPSPs in the train. There was a significant difference between the genotypes in the size of the 3 last pulses in the train (P < 0.05). B: 100 pulses at 10 Hz (WT, n = 6/6; KCC2hy/null, n = 6/6; P < 0.05). C: 100 pulses at 100 Hz (WT, n = 4/3; KCC2hy/null, n = 7/6; P < 0.05). One and 10 Hz: plot represents analysis of fEPSP slope during the train; 100 Hz: plot represents analysis of the fEPSP amplitude from the baseline before tetanization, showing a significant DC shift during the high-frequency stimulation (HFS).

 

Figure 6
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FIG. 6. No differences in the miniature EPSC (mEPSC) amplitudes or intervals between the WT and KCC2hy/null mice. Sample traces of mEPSC recordings from WT (left) KCC2 WT and KCC2hy/null mice. A: cumulative plot and histogram of mEPSC frequencies in WT (10.3 ± 2 event/min) and KCC2hy/null mice (10 ± 2 event/min). B: cumulative plot and histogram of mEPSC amplitudes in WT (13.4 ± 2.1 pA) and KCC2hy/null mice (10.3 ± 0.4 pA).

 





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