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Fig. 3 | Molecular Neurodegeneration

Fig. 3

From: Synaptic and memory dysfunction induced by tau oligomers is rescued by up-regulation of the nitric oxide cascade

Fig. 3

sGC activation protects against the detrimental effect of oTau onto LTP. a The sGC inhibitor ODQ (10 μM, 10 min) blocks the rescue of oTau (100 nM, 20 min) induced LTP reduction by DEA/NO (3 μM, 5 min) (ANOVA: F(1,20) = 2.346, p = 0.141 comparing ODQ + DEA/NO + oTau vs. ODQ; F(1,15) = 0.004, p = 0.954 vs. oTau). The color of the vehicle group is faint because it corresponds to the same group as in B. b Perfusion with BAY41–2272 (100 μM, 10 min) rescued the LTP impairment in slices concomitantly treated with oTau (100 nM, 20 min) in experiments interleaved with those shown in A (BAY41–2272 + oTau: n = 11; ANOVA: F(1,17) = 78.187, p < 0.0001 comparing BAY41–2272 + oTau vs. oTau). BAY41–2272 alone did not modify potentiation (BAY41–2272 alone: n = 11, vs. vehicle: n = 7; F(1,16) = 0.025, p = 0.877). No significant differences were found between tetanized slices treated with BAY41–2272 + oTau or BAY41–2272 (F(1,20) = 4.274, p = 0.052 comparing BAY41–2272 + oTau with BAY41–2272). The color of the oTau group is faint because it corresponds to the same group as in A. c Quantification of the residual potentiation from LTP curves shown in A and B at 30 and 120 min after tetanus. (Vehicle: n = 7 slices/7 animals, 3 males, 4 females; oTau alone n = 8 slices/7 animals, 4 males, 3 females; ODQ: n = 9 slices/8 animals, 4 males, 4 females; ODQ + DEA/NO + oTau: n = 13 slices/11 animals, 6 males, 5 females; BAY41–2272: n = 11 slices/10 animals, 5 males, 5 females; BAY41–2272 + oTau: n = 11 slices/10 animals, 5 males, 5 females). One-way ANOVA: F(5,53) = 14.218, p < 0.0001 at 30 min and F(5,53) = 28.031, p < 0.0001 at 120 min; Bonferroni’s: p < 0.0001 and p < 0.005 between Vehicle and oTau or ODQ or ODQ + DEA/NO + oTau at 30 and 120 min, respectively; p < 0.0001 between oTau and oTau + BAY41–2272 at 30 and 120 min. ***p < 0.005, ****p < 0.0001

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