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. 2020 Dec 4;9:e54838. doi: 10.7554/eLife.54838

Figure 2. Neurexin1α mutants display altered outcome-dependent task engagement.

(A) A proxy of task engagement was measured as the average latency from trial onset (center-light ON) to initiation. Nrxn1α KOs (blue, n = 10) do not exhibit global deficits in task engagement in comparison to WT animals (gray, n = 11) (three-way RM ANOVA). (B) Relative latency to initiate is a standardized comparison of initiation latencies following large rewarded outcomes and small rewarded outcomes within individual animals. (C) Nrxn1α WT mice modulate their trial-by-trial engagement in response to different rewarded outcomes, initiating trials more quickly after large reward outcomes than small reward outcomes. Nrxn1α KOs do not exhibit this outcome-sensitive modulation of task engagement (three-way RM ANOVA). (D and E, top) There is a significant relationship between the ability of WT mice to select actions in response to reward discrepancy (RRS) and their ability to upregulate task engagement (relative initiation latency) which is lost in KOs (D and E, bottom). All data represented as mean ± SEM.

Figure 2—source data 1. Source data for Figure 2.

Figure 2.

Figure 2—figure supplement 1. Additional Task Latency and Reward Volume Data.

Figure 2—figure supplement 1.

(A) Nrxn1α KO mice exhibit extended choice latencies across reward environments. (B) There are no genotypic differences in the total session reward consumption, regardless of reward contrast (left) or probability of feedback (right). (C) There is no significant difference between genotypes in the latency to initiate trials over the course of the 12 µL versus 0 µL sessions (Prew = 0.75). All data analyzed by two-way RM ANOVA. All data represented as mean ± SEM.