Figure 4. Active memory maintenance by the APC delay activity.

(a) Design of the delayed paired association (DPA) task. (b) Correct rates following APC delay-period optogenetic suppression in the DPA task. *, p=0.038, as determined by a mixed-between-within-ANOVA, genotype × laser interaction; error bars represent the 95% confidence intervals of the means from bootstrapping of 1000 repeats. Numbers in brackets show the effect size measured by Cohen’s d for control (in black) and ChR2 (in blue) groups. We noticed some performance variations resulting from DPA optogenetic impairment, and confirmed that there is no outlier with both the 1.5 interquartile ranges and the Grubb’s methods. (c) Behavioral diagram for the dual-task design. (d) Learning curve for the correct rate in the dual-task. Note the drop of DPA performance after inserting the GNG task in the delay period (in red). Arrow, the 4^th day in dual-task training. Light-color traces show the data for individual mice; error bars represent the 95% confidence intervals of the means from bootstrapping of 1000 repeats. (e) Averaged licking rate of mice well-trained for the dual-task in GNG-Go (red), GNG-Nogo (black), DPA-hit (top) and DPA-correct rejection (bottom) trials. Shadows show the 95% confidence interval of the mean from bootstrapping of 1000 repeats. (f) Dual-task interference as illustrated by performance data from the 4^th day of dual-task training. *, p=0.041, one-way repeated measure ANOVA. Gray traces show data for individual mice; error bars show the 95% confidence interval of the mean from bootstrapping of 1000 repeats. (g) DPA-Correct rate after suppressing the APC activity during the later-phase delay period after distractors. P values were obtained from mixed-between-within-ANOVA, genotype × laser interaction; error bars show the 95% confidence intervals of the means from bootstrapping of 1000 repeats. Numbers in brackets represent the effect size as measured by Cohen’s d for control (in black) and ChR2 (in blue) groups. (h) As in (g), but for DPA-false alarm rate. *, p=0.014. See Figure 4—figure supplement 1 for more details for the task performance and control tasks. See Figure 4—figure supplement 2 for optogenetic suppression effect size. See Figure 4—source data 1–2 for complete statistics.

Figure 4—figure supplement 1. Active memory maintenance by the APC delay activity.

(a–d) Miss rate (a), false alarm rate (b), lick efficiency (c) and sensitivity index (d′) (d) following the APC delay-period suppression in the DPA task. *, p=0.018, from the mixed-between-within-ANOVA, genotype × laser interaction; error bars represent the 95% confidence intervals of the means from bootstrapping of 1000 repeats. Numbers in brackets are the effect size measured by Cohen’s d for the control (in black) and ChR2 (in blue) groups. (e–h) Similar to (a–d), but in the dual-task. (i) Design of the dual-task baseline optogenetic control task. (j–n) Correct rate (j), miss rate (k), false alarm rate (l), lick efficiency (m) and d’ (n) in the dual-task DPA task following the APC optogenetic suppression during the baseline period. N.S., statistically not significant result in a mixed-between-within-ANOVA, genotype × laser interaction; error bars represent 95% confidence intervals of the means from bootstrapping of 1000 repeats. Numbers in brackets are the effect size measured by Cohen’s d for the control (in black) and ChR2 (in blue) groups.

Figure 4—figure supplement 2. Optogenetic suppression effect size.

(a–e) Optogenetic effect size, as measured by Cohen’s d, for the correct rate (a), miss rate (b), false alarm rate (c), lick efficiency (d) and sensitivity index (d′) (e) in the single DPA, dual-task DPA and dual-task baseline perturbation control tasks.