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. 2012 Oct 31;32(44):15296–15308. doi: 10.1523/JNEUROSCI.0705-12.2012

Figure 7.

Figure 7.

GluRδ2ho-4J/ho-4J alters the time course of the mGluR1-dependent sEPSC at PF–PC synapses. A, Typical traces of sEPSCs recorded from wild-type or GluRδ2ho-4J/ho-4J mice. Application of the mGluR1 antagonist CPCCOEt blocks sEPSCs. Inset shows corresponding fEPSCs, which are blocked by CNQX. B, GluRδ2ho-4J/ho-4J shows a similar fEPSC input–output relationship as wild type. C, Stimulation intensity for fEPSCs and sEPSCs was set to evoke similar fEPSC amplitudes (∼500 pA). D, The decay constant of fEPSCs was not affected by GluRδ2 mutation. E, The amplitude of sEPSCs was not changed significantly by GluRδ2 mutation. F, The integrated area of the CPCCOEt-sensitive sEPSC was not affected by GluRδ2 mutation. G, The onset of the sEPSC was significantly slowed in GluRδ2ho-4J/ho-4J. The average duration between the stimulus and the peak of the sEPSC was calculated. H, The average FWHM for the CPCCOEt-sensitive sEPSC was calculated. I, FWHM of sEPSC was normalized by the decay constant of fEPSC. The kinetics of sEPSCs was specifically slowed in GluRδ2ho-4J/ho-4J mice. Error bars indicate SEM. C–F, GluRδ2+/+ (n = 18) and GluRδ2ho-4J/ho-4J (n = 11). G–I, GluRδ2+/+ (n = 18) and GluRδ2ho-4J/ho-4J (n = 7). The waveforms of sEPSC in 4 of 11 samples recorded from GluRδ2ho-4J/ho-4J Purkinje cells were too small to evaluate, so we omitted these samples from G–I. J, K, NMDA receptors are not involved in the slower synaptic responses at PF–PC synapses in GluRδ2ho-4J/ho-4J. J, Typical sEPSC traces from wild-type and GluRδ2ho-4J/ho-4J in the presence or absence of 100 μm AP-5. All responses were evoked by five pulses at 100 Hz in the presence of 20 μm bicuculline and 40 μm CNQX. K, Quantified AP-5-sensitive charge transfer. Statistical significance with respect to GluRδ2+/+ (t test). **p < 0.01, ***p < 0.001.