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. 2007 Oct 10;27(41):11056–11064. doi: 10.1523/JNEUROSCI.1941-07.2007

Figure 4.

Figure 4.

Recovery from synaptic depression is delayed in slices from HIP1−/− mice. A, HIP1−/− neurons require more time to recover from synaptic depression in comparison with wild-type littermate controls. CA1 pyramidal cells were voltage clamped at −60 mV and stimulated every 3 s via Schaffer collaterals to obtain baseline synaptic responses in the presence of AP5. A prolonged tetanus (10 Hz, 200 s; bar) was delivered at time 0 to induce synaptic depression including depletion of the readily releasable synaptic vesicle pool. Recovery from depression was studied by recording EPSCs at the original stimulation rate (data were averaged from n = 9 wild-type and n = 6 HIP1−/− neurons). B, Same data as in A were plotted on an expanded time base to compare the initial potentiation of EPSCs during the tetanus demonstrating enhanced facilitation in HIP1−/− mice (mean ± SEM). C, The recovery after synaptic depression is significantly decreased in HIP1−/− neurons in comparison with wild-type neurons. The same data as in A were replotted to show only the synaptic responses at the end of the tetanus and most of the recovery phase. Each point represents six averaged EPSCs ± SEM (t test; *p < 0.05).