Figure 3. Acute Aβ Treatment Increases Surface AMPA Receptor Levels and Excitatory Synaptic Currents.

A–B) Surface levels of GluR1 were assessed by biotinylation assay at 0, 10, 30, or 60 min after addition of Aβ or arachidonic acid (AA) in primary neuronal cultures. Aβ and AA acutely increased surface levels of GluR1 at 10 min, but surface receptor levels returned to baseline after 30 and 60 min of Aβ or AA exposure (B). Inhibiting phospholipase A₂, which releases AA from phospholipids, with AACOCF3 blocked the Aβ-induced increase in surface GluR1 levels (A). C–D) Brain slices were prepared from NTG mice. Neuronal activity was recorded from layer 5 pyramidal neurons in the presence of GABAzine (10 μM). C) Representative spontaneous excitatory postsynaptic currents (sEPSCs) traces recorded from a single voltage-clamped neuron before (left) and 5 min after (middle) application of Aβ, and 7 minutes after washout (right). For each condition, four segments of a continuous trace are shown. Note the increased frequency of sEPSCs after the Aβ treatment. D) Cumulative histograms demonstrating that sEPSC interevent intervals were reversibly decreased by Aβ (left) or AA (middle) and that the Aβ effect could be blocked by AACOCF₃ (right). Adapted from (Sanchez-Mejia et al., 2008).