Figure 7. Pharmacological inactivation of cholinergic signaling decreases VIP- and increases SOM-IN activity during movements in naive mice.

(A) Schematic of the model for learning-related modulation in cortical circuits.

(B) Activity of VIP-INs in the right M1 at the naive stage aligned to the movement onset, with or without local applications of AChR antagonists (775 VIP-INs from 10 mice). Each row represents the activity averaged across trials of individual neurons, sorted according to their activity level during movements within each session. Ctrl.: control sessions, Ant.: manipulation sessions with AChR antagonists.

(C) Activity of VIP-INs averaged across movements and neurons in control and manipulation sessions aligned to the movement onset (mean ± SEM).

(D) Activity during movements averaged across VIP-INs in control and manipulation sessions (p = 0.0024, mixed-effects model, mean ± SEM).

(E) Distribution of changes in the activity level of VIP-INs during movements in the manipulation session compared to the control session.

(F) Fraction of VIP-INs with significant changes in the activity level during movements in the manipulation session compared to the control session at the naive stage.

(G)-(K) Same as (B)-(F) but for SOM-INs (1128 SOM-INs from 11 mice). For (I), AChR antagonists increased the activity of SOM-INs during movements in naive animals, p = 0.0062, mixed-effects model, mean ± SEM.

(L)-(P) Same as (B)-(F) but in naive animals with local applications of only nAChR antagonist in the right M1 (896 VIP-INs from 6 mice). For (N), nAChR antagonist significantly reduced the activity of VIP-INs in naive animals (p = 0.0031, mixed-effects model, mean ± SEM). Ctrl.: control sessions, nAnt.: manipulation sessions with nAChR antagonist.

(Q)-(U) Same as (B)-(F) but with mAChR antagonist (1066 VIP-INs from 7 mice). For (S), mAChR antagonist did not significantly decrease the mean activity of VIP-INs in naive animals (p = 0.2302, mixed-effects model, mean ± SEM). See also Figure S8.