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. 2010 Nov 3;30(44):14835–14842. doi: 10.1523/JNEUROSCI.3030-10.2010

Figure 5.

Figure 5.

Synaptic transmission and plasticity in hippocampal slices. A, Left, Representative fEPSPs recorded in area CA1 of both genotypes when stimulating Schaffer collaterals with increasing stimulation intensities. Right, Input/output relationships 12–15 weeks after induction of the Dicer mutation (each n = 3). B, At 5–6 weeks after induction of mutation, tetanic stimulation [i.e., high-frequency stimulation (HFS)] induced PTP (control, 1.88 ± 0.08, n = 8 slices from 4 mice; mutant, 1.94 ± 0.11, n = 8 slices from 4 mice; p = 0.59) and LTP (control, 1.29 ± 0.05, n = 8 slices from 4 mice; mutant, 1.34 ± 0.08, n = 8 slices from 4 mice; p = 0.62). Bottom, Expanded time course. C, At 12–15 weeks after induction of mutation, PTP was higher in the mutant than in control (PTP: control, 1.76 ± 0.10, n = 8 slices from 3 mice; mutant, 2.39 ± 0.14, n = 8 slices from 3 mice; p < 0.01; LTP: control, 1.34 ± 0.05, n = 8 slices from 3 mice; mutant, 1.39 ± 0.08, n = 8 slices from 3 mice; p = 0.6). D, At 12–15 weeks after induction of mutation, repeated HFS induced higher PTP each time after HFS, but LTP remained comparable in both genotypes (control, 1.84 ± 0.1, n = 9 slices from 3 mice; mutant, 1.98 ± 0.13, n = slices from 3 mice; p = 0.41). In both genotypes, four times HFS induced higher LTP than single HFS (p < 0.05). The traces show the mean of 45 and 30 consecutive fEPSPs before and 40–50 min after single HFS in both genotypes, respectively. TAM, Tamoxifen.