Fig. 6
Aβ-mediated somatic potentiation of dendritic inputs. a Illustration of the stimulating and recording paradigm. Patch-clamp recordings were performed in the current-clamp mode either at the soma or at the dendrite (200 μm distance from the soma) proximal to the stimulating electrode. b Averaged sample traces recorded at the soma, showing EPSPs before and after Aβ1–42 peptide (500 nM) treatment. Potentiation of EPSPs was only detected when patch recording was performed at the soma, but not at the dendrite. c–f Graphs showing the time course and magnitude of the change in normalized EPSPs recorded at the soma (c, d) and at the dendrite where synaptic inputs were activated by stimulating electrode (e, f). d, f Summary of results from all experiments as that shown in (c) and (e), respectively. g Illustration of local application (pressure puffing) of GluN2B-NMDAR blocker ifenprodil (3 μM) to the soma. Whole-cell patch-clamp recording was performed at the soma while stimulation was delivered at the dendrite. h Aβ1–42-induced EPSP potentiation was reversed by the GluN2B-NMDAR blocker ifenprodil (3 μM) that was locally applied to the soma. Ifenprodil (3 μM) was applied 2 min after Aβ1–42 (500 nM) treatment. i Statistical histogram showing the dependency of the Aβ1–42-induced EPSP potentiation on the activity of somatic GluN2B-NMDARs. j Effects of Aβ1–42 at different concentrations on the potentiation of synaptic inputs. k Summarized dose–response data. l Similar potentiation effects produced by 100 nM TBOA and 500 nM Aβ1–42. Data are means ± SEM, **P < 0.01, t test; ns, no significance