In slices treated with vehicle, this stimulation protocol did not produce a change in eIPSC amplitude from baseline, whereas there was a marked and lasting reduction in eIPSC amplitude in AM3506-pretreated slices (ANOVA effect of treatment: F1,44 = 469.30, P<0.01, n = 7–8) (Figure 2e). These data demonstrate that AM3506 enhances LTDi in the amygdala and echo the previous observation that a similar effect is produced by brain-wide gene deletion of faah in mice.56 PPR, which measures the peak change in eIPSC amplitude over two consecutive stimulations (for traces see Figure 2e), was increased in AM3506-treated slices after LFS, relative to baseline (t-test: t(4) = 4.33, P<0.05, n = 5) (Figure 2f, for traces see Figure 2e). Because alterations in PPR are typically associated with a change in presynaptic release probability, these data suggest that AM3506 promoted activity-dependent suppression of GABA release.
