Extended Data Fig. 5: Optogenetic inhibition of callosal PV terminals (but not nonspecific inhibition of all callosal terminals) increases errors during rule shifts.
From: Long-range inhibition synchronizes and updates prefrontal task activity
a, e, i, m, Experimental design: Day 1, no light delivery; Day 2, continuous light for optogenetic inhibition of callosal PV terminals during the rule shift (RS). b, f, j, n, Representative image showing viral expression in the mPFC ipsilateral to the injection (ipsi), and labeled callosal terminals in the contralateral mPFC (contra). c, g, Optogenetic inhibition of callosal PV terminals increases perseverative errors in DIO-eNpHR mice (n = 8 mice) compared to DIO-eYFP controls (n = 7 mice; two-way ANOVA (task day × virus); interaction: F(1,13) = 35.71, P < 0.0001). d, h, Optogenetic inhibition of callosal PV terminals has a marginal effect on random errors in DIO-eNpHR mice (n = 8 mice) compared to DIO-eYFP controls (n = 7 mice; two-way ANOVA (task day × virus); interaction: F(1,13) = 4.617, P = 0.0511). c, d, Light delivery does not affect the number of perseverative (post hoc t(13) = 1.877, P = 0.1662) or random (post hoc t(13) = 0.0, P > 0.9999) errors in DIO-eYFP controls. g, h, Optogenetic inhibition of callosal PV terminals on Day 2 increased the number of perseverative (post hoc t(13) = 10.75, P < 0.0001) and random (post hoc t(13) = 3.145, P = 0.0155) errors compared to no stimulation on Day 1. k, l, o, p, Optogenetic inhibition of all callosal projections has no effect on perseverative errors in Syn-eNpHR mice (n = 6) compared to controls (n = 4; two-way ANOVA (task day × virus); interaction: F(1,8) = 0.0, P > 0.9999) nor on random errors (two-way ANOVA (task day × virus); interaction: F(1,8) = 0.07805, P = 0.787). Two-way ANOVA followed by Bonferroni post hoc comparisons was used. *P < 0.05, ****P < 0.0001; scale bars, 250 μm and 100 μm, respectively.
