CP- and CI-AMPARs are eliminated via different conditioning protocols. A, EPSP amplitude time course (mean ± SEM) before and after burst conditioning (□) that led to significant EPSP depression (p < 0.005). Bath-applied PhTx (5 μm) at the end of the experiment left EPSPs unaltered (p > 0.5). Top, Sample EPSPs in control (1) and after conditioning (2); sample burst (□). B, Current–voltage relationship and sample traces of conditioned EPSCs recorded in a representative experiment by repatching the neuron with a Cs⁺ solution. C, Summary histogram for RI (mean ± SEM) in control and after conditioning. Both values were significantly different (**p < 0.0005). D, Similar experiment to that in A with the PKC inhibitor 19–31 (0.5 μm) added intracellularly. Burst conditioning (□) led to significant LTD (p < 0.005). PhTx was bath applied toward the end of the experiment without affecting the EPSPs (p > 0.1). Sample EPSPs for control (1), after conditioning (2), and PhTx (3) are illustrated above. E, Analogous experiment with the GluR2-specific inhibitory peptide SVKI (0.2 mm) in the pipette. Burst conditioning (□) still induced significant LTD (p < 0.005). F, Burst conditioning (□) in the presence of bath-applied H9 (0.5 mm), a broad-spectrum protein kinase inhibitor, induced significant LTD (p < 0.005). Top, Sample EPSPs in control (1) and after conditioning (2). G, Burst conditioning (□) with the PP1/2A inhibitor okadaic acid (0.1 μm) in the pipette left EPSPs unaltered (p > 0.5). However, PhTx that was bath applied after the conditioning significantly diminished the EPSPs (p < 0.05). Above sample EPSPs in control (1), after conditioning (2), and in PhTx (3).