Fig. 2

oTau induced LTP impairment was rescued by the NO donor DEA/NO. a LTP was impaired in hippocampal slices from mice perfused for 20 min before tetanus with 100 nM oTau compared to vehicle-treated slices (ANOVA for repeated measures: F_(1,19) = 30.859, p < 0.0001). A perfusion with DEA/NO (3 μM, 5 min) rescued the LTP impairment in slices concomitantly treated with oTau (100 nM, 20 min) in experiments that were interleaved with those shown in A (ANOVA for repeated measures: F_(1,23) = 31.208, p < 0.0001 comparing tetanized slices treated with oTau + DEA/NO vs. oTau). No differences were found between tetanized slices treated with DEA/NO alone vs. DEA/NO + oTau (F_(1,26) = 0.052, p = 0.821) and DEA/NO alone did not modify potentiation (DEA/NO vs. vehicle: F_(1,22) = 0.155, p = 0.697). Upper panel: representative traces of fEPSP before (gray) and after tetanus (black) for experiments shown in A. b Basal neurotransmission was not affected by oTau, DEA/NO or DEA/NO + oTau in slices that were not tetanized compared with slices treated with vehicle (F_(3,16) = 0.950, p = 0.440; n = 5 slices from 5 animals, 3 males and 2 females for each condition). c Quantification of the residual potentiation at 30 and 120 min after tetanus (average of the last 5 min recording from LTP data shown in a and b). Vehicle: n = 10 slices/8 animals, 4 males and 4 females; oTau: n = 11 slices/8 animals, 4 males and 4 females; DEA/NO: n = 14 slices/12 animals, 6 males and 6 females; DEA/NO + oTau: n = 14 slices/11 animals, 6 males and 5 female. One-way ANOVA among all: F_(3,45) = 1.124, p < 0.0001 at 30 min; F_(3,35) = 28.180, p < 0.0001 at 120 min. Bonferroni’s: p < 0.0001 between oTau and other experimental conditions at 30 min and 120 min. The horizontal bars indicate the period during which drugs were added to the bath solution, and arrows indicate tetanus delivery here and in the following figures. ****p < 0.0001