The Journal of Neuroscience, July 18, 2007, ():
Aß Oligomer-Mediated Long-Term Potentiation Impairment Involves Protein Phosphatase 1-Dependent Mechanisms
J. Neurosci. Knobloch et al.
27: 7648
Supplemental Data
Files in this Data Supplement:
- supplemental material
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Supplementary figure 1
Passive immunization with an antibody against the Aβ-sequence partially rescues the LTP deficit in slices from 3.5 months-old arcAβ mice (p<0.01, repeated measurement ANOVA, tg anti-Aβ antibody vs. non-treated tg; 85% ± 4.5% level of potentiation of wt slices,) whereas immunization with a control antibody has no effect (p=0.6, repeated measurement ANOVA, tg control antibody vs. non-treated tg). Basal transmission is not affected (right inset). Individual fEPSP traces before (black) and after (red) LTP induction are presented in left insets (n=3tg mice immunized with anti-Aβ antibody, n=3tg mice immunized with control antibody). Scale bar = 0.6mV/5ms.
- supplemental material
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Supplementary figure 2
Representative Western blots showing the level of phosphorylated and total CaMKII in crude synaptic membrane preparations from arcAβ mice and wildtype littermates. Densitometric analysis revealed a reduction in the phosphorylation level of CaMKII in tg mice (ratio phospho/total, Mann Whitney-U, p=0.08).
