(A) Neurexin1α was conditionally inactivated in thalamic progenitor cells by crossing the Neurexin1α-conditional knockout line onto the Olig3-Cre line. (B) Coronal section of Olig3Cre; Ai14 reporter cross showing expression of tdTOM broadly throughout thalamic nuclei. (C) RT-qPCR of RNA from adult mouse thalamus (n = 2 for Nrxn1αfl/fl;Olig3+/+ (gray); n = 3 for Nrxn1αfl/fl;Olig3Cre/+(orange)). Cre-mediated recombination results in reduced expression of Nrxn1α mRNA detected by exon 9 probe (two-sample t-test: p<0.0001) and moderate nonsense-mediated decay (two-sample t-test: p<0.001) (D) Nrxn1αfl/fl;Olig3Cre/+ mutant animals (orange; n = 10) do not exhibit changes in relative reward-stay in comparison with Nrxn1αfl/fl;Olig3+/+(gray; n = 8) control animals. (E–G) Nrxn1αfl/fl;Olig3Cre/+ mutant mice do not have a deficit in updating or representing choice values (two-way RM ANOVA). (H–J) Nrxn1αfl/fl;Olig3Cre/+ mutants exhibit a normal relationship between choice values and decision behavior. (K–M) Nrxn1αfl/fl;Olig3Cre/+ mutants do not exhibit a deficit in the allocation of choices guided by relative choice costs (K, two-way RM ANOVA, left; two-sample t-test, right, p>0.05). Mutants exhibit no difference in task engagement (L, p>0.05) or in choice latencies (M, p>0.05). All data represented as mean ± SEM.
Figure 6—source data 1. Source Data for Figure 6.