Figure 5

Ubc9 transduction rescues Aβ-induced deficits in long-term potentiation.

(a) Hippocampal slices were treated with vehicle (PBS), TAT-Ubc9, Aβ₄₂ oligomers or Aβ plus TAT-Ubc9 prior to stimulation by high potassium. Representative western blots show high molecular weight SUMO2/3 conjugation. Vehicle n = 11 each non-stimulated and stimulated, TAT-Ubc9 n = 3 each, Aβ n = 6 each, Aβ plus TAT-Ubc9 n = 6 each. ANOVA p = 0.005; *p < 0.05 versus all other groups. (b) LTP in area CA1 of hippocampal slices induced by theta burst stimulation of Schaffer collaterals. Perfused treatments were prior to LTP induction and include: vehicle (PBS), TAT-Ubc9 (50 nM) for 1 hour, Aβ₄₂ oligomers (200 nM) for 20 minutes, or combined Aβ plus TAT-Ubc9. Vehicle n = 15, TAT-Ubc9 n = 9, Aβ n = 14, Aβ plus TAT-Ubc9 n = 9. (c) Quantification of the last 10 minutes of LTP recordings. ANOVA of the averages of the last 10 minutes p = 0.002; *p < 0.05 versus all other groups. (d) LTP with hippocampal slices from Tg2576 mice. Perfused treatments were prior to LTP induction and include: vehicle (PBS) or TAT-Ubc9 (50 nM) for 1 hour. WT vehicle n = 10, WT TAT-Ubc9 n = 13, APP vehicle n = 14, APP TAT-Ubc9 n = 15. (e) Quantification of the last 10 minutes of LTP recordings. ANOVA of the averages of the last 10 minutes p = 0.001; *p < 0.05 versus all other groups. Data presented as means ± SEM. See also Supplementary Figure S5.