Figure 7. Calcium/calmodulin-dependent kinase II (CaMKII) inhibition in somatostatin (SST) interneurons during the first visuomotor experience reduced visually driven inhibition.
(A) Mean correlation between neuronal activity and visual flow in the open-loop condition for all L2/3 excitatory neurons recorded in adult control, ΔGrin1adult, ΔGrin1juv, paAIP2CaMKIIα, paAIP2SST, and paAIP2PV mice. Error bars indicate the standard error of the mean (SEM) across neurons. Dashed black line and corresponding gray shading indicate the mean correlation of activity and visual flow and SEM of the adult control group; gray shading indicates SEM across neurons. Comparison against adult control data: n.s.: p>0.05, **p<0.01, ***p<0.001. For all details of statistical testing, see Supplementary file 1A. (B) Through visuomotor experience, local plasticity in V1 establishes a balance between top-down and bottom-up input in L2/3 neurons (Jordan and Keller, 2020), which is thought to drive prediction error responses. In this model, we refer to neurons that receive strong bottom-up excitation and strong top-down inhibition as positive prediction error (PPE) neurons, while those that receive strong top-down excitation and strong bottom-up inhibition, we refer to as negative prediction error (NPE) neurons. Given that interfering with plasticity in either excitatory neurons or SST interneurons prevents normal development of visual responses in excitatory neurons, combined with the finding that visual responses in neither population of neurons depend on coupled visuomotor experience (Attinger et al., 2017), we conclude that visual experience is necessary and sufficient for shaping visual inputs onto both populations of neurons. As mismatch responses in excitatory neurons depend on visuomotor experience and are sensitive to blocking plasticity in excitatory neurons, the proper wiring of top-down input onto L2/3 excitatory neurons likely requires coupled visuomotor experience. SST interneurons likely mediate visually driven inhibition, and we speculate that they also mediate the top-down motor-related inhibition. The effect of interfering with plasticity in parvalbumin (PV) interneurons is consistent with the idea that they regulate overall gain of the circuit.