The Journal of Neuroscience, July 20, 2005, ():
Amyloid-
Peptide Inhibits Activation of the Nitric Oxide/cGMP/cAMP-Responsive Element-Binding Protein Pathway during Hippocampal Synaptic Plasticity
J. Neurosci. Puzzo et al.
25: 6887
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Files in this Data Supplement:
- Supplemental Fig. 1
-
NO rescues A?-induced impairment of LTP induced with a 1 ten-burst train
Oligomeric A?1-42 (200 nM) for 20 min reduces LTP induced with a single tetanic stimulation including 1 ten-burst train (99.06 ± 14.20% vs 161.63 ± 18.07% of baseline slope at 120 minutes, n=4/4, F(1, 6)=8.28, p<0.05). DEA/NO reverses the A?-induced LTP impairment (189.97 ± 26.84% of baseline slope at 120 minutes, n=4, F(1, 6)=8.77, p<0.05 compared to A?+tetanus). Similar results were obtained with 8-Br-cGMP (162.58 ± 25.71% of baseline slope at 120 minutes, n=4, F(1, 6)=7.21, p<0.05 compared to A?+tetanus; data not shown). As previously described (Lu et al, 1999), DEA/NO and 8-Br-cGMP alone increased the amounts of potentiation (221.51 ± 14.20% and 220.89 ± 11.42%, n=4 for both, F(1, 6)=11.05 and F(1, 6)=9.02, p<0.05 compared to one tetanus).
- Supplemental Fig. 2
-
Scramble A?1-42 does not modify LTP
Scramble A?1-42 does not modify LTP (201.579 ± 12.86% vs. 209.11 ± 15.06% of baseline slope at 120 minutes after tetanus, n=4/5; F(1, 7)=0.22, p>0.1 compared to tetanized slices treated with vehicle alone) and baseline transmission (101.11 ± 1.28 vs. 98.75 ± 1.96% of baseline slope at 120 minutes after tetanus, n=4/4; F(1, 6)=0.14, p>0.1 compared to control slices).
