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Facilitation of AMPA Receptor Synaptic Delivery as a Molecular Mechanism for Cognitive Enhancement

Figure 6

FGL enhances long-term synaptic potentiation.

(A–B) Rectification experiments similar to the ones described in Figure 5, after incubation with DL-AP5 (NMDAR inhibitor), KN-93 (CaMKII inhibitor), or KN-92 (inactive analog of KN-93). Sample traces are shown above the graphs. (C) Sample traces of evoked AMPAR-mediated synaptic responses recorded from CA1 neurons at −60 mV before (thin line) and after (thick line) LTP induction. LTP was induced by pairing presynaptic 3 Hz stimulation (540 pulses) with postsynaptic depolarization (0 mV). One of the stimulating electrodes was turned off during LTP induction (“unpaired pathway”). Organotypic slice cultures were incubated with (i) normal culture medium (control), (ii) FGL, (iii) the PKC inhibitor chelerythrine (Chel), or (iv) FGL and chelerythrine (FGL+Chel), as indicated. Treatments were for 24 h and slices were transferred to fresh culture medium (without FGL or chelerythine) for an additional 24 h prior to recordings. (D) Time course of normalized AMPAR-mediated synaptic responses before and after LTP induction (black arrow), from the slices treated as in (C). For simplicity, each time point in the plot corresponds to the average of 12 consecutive stimulations (sampling rate: 0.2 Hz). (E–F) Quantification of average synaptic potentiation from paired (“LTP”) and unpaired pathways from the last 10 min of the time-course shown in (D). The p value was determined with the Mann-Whitney test. N, number of cells.

Figure 6