Receptor for Advanced Glycation End Product-Dependent Activation of p38 Mitogen-Activated Protein Kinase Contributes to Amyloid-β-Mediated Cortical Synaptic Dysfunction

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Figure 1.
Figure 1.

Inhibitory effect of Aβ42 on LTP in entorhinal cortex slices. A, Schematic drawing of entorhinal cortex slices and position of electrodes (stimulus position in layer II, recording pipette in layer II/III). MEC, Medial entorhinal cortex; LEC, lateral entorhinal cortex; DG, dentate gyrus; SUB, subiculum. B, Representative field potentials recorded before and 50 min after HFS in vehicle-treated slices and in slices treated with Aβ42 (200 nm). Calibration: 1 mV, 5 ms. Under control conditions LTP expression is induced by HFS, applied after 15 min of baseline recording. C, LTP was induced by HFS stimulation in vehicle-treated slices (open circles), whereas LTP expression was blocked by bath application of Aβ42 (200 nm, gray circles) for 10 min (dark bar). D, No effect on LTP expression was observed in the presence of reversed peptide Aβ (42–1, 200 nm, open squares) or a low concentration of Aβ42 (20 nm, filled squares). E, Input–output curves. The relative amplitude (Rel. Amp.) as a function of stimulus intensity (Stim. Int.) measured in volts (V) did not show significant differences between vehicle-treated (open circles) and Aβ42-treated slices (gray circles). F, Paired-pulse facilitation. Paired-pulse-induced change was calculated as the ratio of the peak amplitude of the second evoked field potential to the first one (PP ratio) for different interstimulus intervals (25–200 ms). PP ratio was not modified in Aβ42 (200 nm, gray circles) treated slices respect to vehicle-treated slices (open circles). Error bars indicate SEM.

  1. The Journal of Neuroscience vol. 28 no. 13 3521-3530
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