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    • br Experimental procedures br Results

    2020-08-06


    Experimental procedures
    Results Experiment 1: SERT−/− rats show no fear-potentiated startle. With both shock intensities, genotypes differed in their response to cued and non-cued trials (trial×genotype interaction: [F2,42=4.9, p<0.05 and F2,52=8.9, p<0.001 for 0.3 and 0.6mA respectively]): SERT+/+ and SERT+/− showed significant potentiation of the startle response whereas SERT−/− did not (SERT+/+: F1,11=12.4, p<0.01, SERT+/−: F1,15=18.6, p=0.001, SERT−/−: F1,16=1.2, NS; Figure 1A and B). The response to non-cued trials was increased in SERT−/− following 0.6mA, but not 0.3mA FPS training. However, this effect did not reach significance (effect Toremifene on non-cued trials [F2,42<1] and [F2,52=2.8, p<0.1] for 0.3 and 0.6mA respectively). The blunted FPS response in SERT−/− under both shock intensities was also reflected in a significantly lower percentage FPS (Effect of genotype [F2,42=6.5, p<0.01] and [F2,52=4.4, p<0.05] for 0.3 and 0.6mA respectively, Figure 1C and D). Experiment 2: Blunted fear-potentiated startle due to deficient fear acquisition. SERT+/+ and SERT+/− showed significant acquisition of the cue-shock association, whereas SERT−/− did not (trial×genotype interaction: F2,50=3.3, p<0.05; effect of trial: SERT+/+F1,17=10.1, p<0.01; SERT+/−F1,18=5.0, p<0.05; and SERT−/−F1,15<1, Figure 2A and C). In addition, whereas SERT+/+ differentiated between cued and non-cued trials during both the first and second phase of acquisition (1st phase [T1,17=−2.6, p<0.05], 2nd phase [T1,17=−3.0, p<0.01]), SERT+/− only differentiated between cued and non-cued trials during the first phase of acquisition (1st phase [T1.18=−2.9, p<0.001], 2nd phase T1,18=−1.7, NS]). The response to non-cued trials increased over time independently of genotype [phase×genotype interaction and overall effect phase on non-cued trials F4,106<1 and F2,106=36.6, p<0.001]. Experiment 3: Neither acute nor chronic pharmacological SERT inhibition affects the acquisition and expression of fear-potentiated startle. Acquisition: Following fear acquisition significant FPS was induced (Effect of trial [F1,30=39.3, p<0.001] and [F1.32=32.0, p<0.001] in acute and chronic group respectively) and neither acute nor chronic paroxetine treatment significantly affected the level of fear acquisition, as measured 24h later ([drug×trial interaction F1,30<1 and F2,32<1 in acute and chronic group respectively]; Figure 3A and C). Rather, acute paroxetine treatment during acquisition increased overall startle responding 24h later [main effect dose F1,30=3.6, p<0.05], an effect that was primarily mediated by the 10mg/kg dose [p=0.053]. Expression: Neither acute nor chronic paroxetine treatment affected the expression of FPS in pre-trained rats (trial×dose interaction F2,30<1 for both time points; Figure 3B and D). Significant FPS was established at both time points measured (Effect of trial [F1,30=19.0, p<0.001] and [F1,30=21.6, p<0.001] for acute and chronic treatment respectively).