Extended Data Fig. 8: Manipulation of PVGPe-PF but not PVGPe-SNr neurons rescues behavioral flexibility deficit in dopamine-depleted mice.
From: Divergent pallidal pathways underlying distinct Parkinsonian behavioral deficits
a, Number of errors during the reversal-learning phase made by mice that received chemogenetic inhibition in PVGPe-PF neurons after dopamine depletion (n = 7 mice for eGFP-vehicle, n = 7 mice for eGFP-OHDA, and n = 7 mice for hM4Di-OHDA). Left, perseverative errors; One-way ANOVA, F(2,18) = 0.9771, p = 0.3955. Right, regressive errors; One-way ANOVA, F(2,18) = 5.595, p = 0.0129; Bonferroni’s post hoc test, *p = 0.0312 (eGFP-vehicle vs. eGFP-OHDA) and 0.0267 (eGFP-OHDA vs. hM4Di-OHDA). b, Performance of mice that received photostimulation in PVGPe-SNr neurons after dopamine depletion (n = 6 mice for eGFP-vehicle, n = 4 mice for eGFP-OHDA, and n = 6 mice for oChIEF-OHDA). Left, dopamine depletion did not affect performance in the association phase. One-way ANOVA, F(2,13) = 0.8222, p = 0.4611. Right, activation of PVGPe-SNr neurons during reversal learning did not improved behavioral flexibility in dopamine-depleted mice. One-way ANOVA, F(2,13) = 11.69, p = 0.0012; Bonferroni’s post hoc test, **p = 0.0032 (eGFP-vehicle vs. eGFP-OHDA) and 0.0042 (eGFP-vehicle vs. oChIEF-OHDA). c, Number of errors during the reversal-learning phase made by mice in c. Left, perseverative errors; One-way ANOVA, F(2,13) = 1.308, p = 0.3038. Right, regressive errors; One-way ANOVA, F(2,13) = 0.6464, p = 0.54. All data presented as mean ± SEM.
