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. 2017 Apr 18;18(6):962–981. doi: 10.15252/embr.201643519

Figure 3. An agonist of dopamine D1/D5 receptors selectively rescues late LTP impaired by Aβ1‐42, but not Aβ3(pE)‐42.

Figure 3

  • A–C
    (A) Schematic representation of electrode positioning in acute hippocampal slice. LTP recordings revealed that both (B) Aβ1‐42 (n = 8) and (C) Aβ3(pE)‐42 (n = 7) cause impairment of late phase LTP compared to control measurements (n = 8).
  • D
    Basal synaptic transmission is not affected by bath application of Aβ1‐42 (n = 8) or Aβ3(pE)‐42 (n = 7) oligomers.
  • E
    Basal synaptic transmission is not affected by dopamine D1/D5 receptor agonist SKF38393 (n = 7) applied alone or together with Aβ oligomers (n = 7 in each group).
  • F
    Application of SKF38393 in control conditions does not alter tetanisation‐triggered LTP.
  • G, H
    Activation of D1/D5 receptors by SKF38393 restores the CA1 LTP in Aβ1‐42‐treated (n = 7), but not Aβ3(pE)‐42‐treated slices (n = 7).
  • I
    Dot plot representing averaged fEPSP slope. P‐values versus control by one‐way ANOVA.
Data information: All data come from the same experiments where a group of slices were treated with oligomers with or without SKF38393. n corresponds to the number of slices from at least three mice. Data are represented as mean ± s.e.m.