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. 2012 Dec 3;123(1):348–361. doi: 10.1172/JCI64650

Figure 2. Restoration of adult neurogenesis rescued newborn neuron–dependent synaptic plasticity in the DG of Ts65Dn mice.

Figure 2

fEPSPs in the DG medial molecular layer elicited through the stimulation of the MPP in ACSF were recorded in hippocampal slices obtained from Ts65Dn and WT mice fed with normal or lithium-containing diets for either 1 or 4 weeks. (A) Position of the stimulating and recording electrodes. (B) ACSF-LTP was induced in hippocampal slices from saline-treated WT (P < 0.01 vs. baseline) but not Ts65Dn mice (P = 0.190). (C) ACSF-LTP was restored in hippocampal slices of Ts65Dn mice (P < 0.01) and increased in slices from WT littermates (P < 0.01) after 4 weeks of lithium treatment. (D) ACSF-LTP was inhibited through the specific NR2B antagonist Ro25-6981 (1.5 μM) in hippocampal slices from WT (P = 0.469) and Ts65Dn (P = 0.091) mice treated with lithium for 4 weeks. (E) ACSF-LTP was induced in hippocampal slices of WT (P < 0.001) but not Ts65Dn (P = 0.802) mice treated with lithium for only 1 week. The insets in B–E show representative fEPSP traces recorded 5 minutes before (black) and 45 minutes after (gray) LTP induction. (F) Quantification of ACSF-LTP elicited in the DG of WT and Ts65Dn mice. Numbers in parentheses indicate the number of slices recorded for each experimental group. 2-way ANOVA: genotype (F1,43 = 16.721, P < 0.001), treatment (F3,43 = 25.431, P < 0.001), genotype × treatment (F3,43 = 4.996, P = 0.005). *P < 0.05; **P < 0.01, Tukey’s post hoc test.