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. Author manuscript; available in PMC: 2008 Sep 9.
Published in final edited form as: Nat Neurosci. 2008 Apr 6;11(5):547–554. doi: 10.1038/nn.2100

Figure 5.

Figure 5

Hippocampi from mice lacking one copy of Synj1 show normal LTP in the presence of oAβ42. (a) Left, representative western blot analysis of synaptojanin 1 and tubulin in adult Synj1+/+ and Synj1+/− brain extracts (50 μg). Right, quantitative analysis of the blots (n = 4, P < 0.05). (b) PtdIns(4,5)P2 levels in cortical cultures from Synj1+/+ and Synj1+/− mice after a 2-h treatment with 200 nM oAβ42. Although levels of PtdIns(4,5)P2 were reduced by oβ42 in Synj1+/+ cultures (P < 0.05), the levels of this lipid in Synj1+/− neurons were unaffected by the peptide (P = 0.853) (n = 8 and n = 6 in control and oAβ42-treated cultures from Synj1+/+ mice, respectively; n = 9 and n = 6 in control and oAβ42-treated cultures from Synj1+/− mice, respectively). (c) Although Synj1+/+ slices (n = 7) showed a reduction of LTP following bath application of 200 nM oAβ42 (F1,15 = 8.556, P = 0.0104, relative to vehicle), Synj1+/− slices (n = 7) showed normal LTP in the presence of the peptide (F1,16 = 0.121, P = 0.73, relative to vehicle). LTP was normal in Synj1+/− slices (n = 11) compared to Synj1+/+ slices (n = 10) in the presence of vehicle (F1,19 = 0.026, P = 0.87). Basal synaptic transmission was not affected in the Syn1+/− mice (Supplementary Fig. 6). fEPSP, CA1 field-excitatory postsynaptic potential. The bar represents the time of bath application of oAβ42. The three arrows represent the θ-burst stimulation used to induce potentiation. Animals were 3–4 months old.