Fig. 2: PVT→NAc activity dynamics are necessary and sufficient for the expression and suppression of sucrose self-administration and seeking.
From: An opioid-gated thalamoaccumbal circuit for the suppression of reward seeking in mice
a–c Surgical strategy (a) for optogenetic manipulation of PVT→NAc neurons (b) during sucrose self-administration (c; image modified from Vollmer et al.71). d Raster plot showing example active lever pressing rates in each group during sucrose self-administration (examples from 5 mice/group; yellow bar = light on). e Group data showing that optogenetic stimulation of PVT→NAc neurons suppressed active lever pressing (n = 8 eYFP, 8 eNpHR, 9 ChR2 mice; repeated-measures two-way ANOVA, day × group interaction: F2,22 = 7.09, P = 0.004; Sidak’s post-hoc: P = 0.006). f–h TMT (f), yohimbine (g), and extinction (h) suppressed active lever pressing, whereas inhibition of PVT→NAc neurons in eNpHR mice rescued active lever pressing (TMT: n = 8 eYFP, 9 eNpHR, 9 ChR2 mice; repeated-measures two-way ANOVA, day × group interaction: F2,23 = 5.36, P = 0.01; Sidak’s post-hoc: eYFP P = 0.009, ChR2 P = 0.001; yohimbine: n = 8 eYFP, 9 eNpHR, 8 ChR2 mice; repeated-measures two-way ANOVA, day effect: F1,22 = 20.46, P = 0.002; Sidak’s post-hoc: eYFP P = 0.002, ChR2 P = 0.04; extinction: n = 8 eYFP, 9 eNpHR, 9 ChR2 mice; repeated-measures two-way ANOVA, day × group interaction: F2,23 = 19.55, P < 0.001; Sidak’s post-hoc: P < 0.001). i Cue-induced reinstatement of active lever pressing after extinction was abolished by stimulation of PVT→NAc neurons in ChR2 mice (n = 8 eYFP, 8 eNpHR, 9 ChR2 mice; repeated-measures two-way ANOVA, day × group interaction: F2,22 = 6.15, P = 0.008; Sidak’s post-hoc: eYFP P = 0.007, eNpHR P = 0.001). Ext extinction, Opto optogenetic manipulation, SA self-administration. Group comparisons: *P < 0.05, **P < 0.01, ***P = 0.001, ****P < 0.001. Bar graphs are presented as mean ± SEM. Source data are provided as a Source Data file.
