Fig. 6
Aβ1–42 inhibits ex vivo hippocampal LTP and induces LTD in both female and male mice. A–C I/O curve with paired fEPSPs collected at increasing stimulus intensities (from 0.075 to 0.4 mA) from control vehicle (A), Aβ1–42 (B) and Aβ42–1 reverse control (C) slices, respectively. Data is expressed as a percentage (%) of the maximum amplitude obtained. D PPF curve with paired fEPSPs collected at interstimulus intervals of 10, 20, 40, 100, 200 and 500 ms. Data is expressed as mean ± SEM amplitude of the second fEPSP as a percentage of the first [(second/first) × 100] for each inter-pulse interval used. E Representative averaged (n = 5) traces of fEPSPs recorded in the CA1 area, collected during the baseline (1) and ≈50 min post-HFS (2) in hippocampal slices from the different groups. F Time course of LTP evoked in the CA1 area after HFS in hippocampal slices from the different groups. Recordings were obtained from day 1 to 17 post-icv. injection. G, H Bars illustrate mean ± SEM fEPSPs amplitude of the last 10 min of the recording, to show acute (G; 24–48 h post-icv. injection) vs. long-term (H; 3–17 days post-icv. injection) effects on LTP. N (slices) vehicles: males = 6–5 and females = 5–5; N Aβ1–42: males = 7–7 and females = 6–7; N reverse Aβ42–1: males = 5–7 and females = 6–7. Aβ, amyloid-β; HFS, High frequency stimulation; LTP, long-term potentiation; mA, milliamperes; ms, milliseconds; min, minutes. ***p < 0.001 vs. vehicle of the corresponding sex; ###p < 0.001 vs. Aβ42–1 of the corresponding sex