Fig. 1
From: Differential vulnerability of hippocampal CA3-CA1 synapses to Aβ
Human Aβ1-42 blocks b-LTP in wild-type, but not Mapt−/− mice. a EPSPs were evoked with two electrical stimulation electrodes (stim 1 and stim 2). Each electrode activated an independent pathway (test or control pathway, respectively) of hippocampal Schaffer collateral (coll.) and commissural (comm.) projections to CA1 pyramidal neurons in WT mice (b) and Mapt−/− mice (c). After a 10-min baseline, the burst timing-dependent plasticity protocol was applied to one of these pathways (test pathway; black and red symbols) while the other pathway served as control (control pathway; gray and pink symbols). Both test and control pathways were monitored for a further 35 min. Recordings were made in aCSF following incubation for 1–3 h in 220 nM hAβ1-42 (hAβ1-42; red and pink) or vehicle control (control; black and gray). Representative EPSP traces are from the test pathway in hAβ1-42 (red) and control aCSF (black) at the indicated time points (1. Baseline, prior to the induction protocol, 2. At the end of the recording). d The mean of the normalized EPSP slope during the last five minutes of recording (30–35 min post-pairing; mean for control pathway not shown) was used as the outcome measure. Following two-way ANOVA (see text), significance was tested with post-hoc corrected Student’s t-tests. Error bars are SEM. *P < 0.05