miR-132, an experience-dependent microRNA, is essential for visual cortex plasticity

In vivo inhibition of miR-132 in V1 neurons disrupts their ocular dominance plasticity. (a) Top left, schematic of experimental design. Top right, confocal microscopy images showing mCherry expression in cortical layers 1–3 at P28 following neonatal injection (arrow) of mCherry–miR-132 sponge–expressing lentivirus. Bottom, two-photon microscopy image showing mCherry expression alone (left) and its overlay with OGB (green) fluorescence (right) in an injected mouse that underwent monocular deprivation; selected neurons used in b are circled and numbered. Scale bars represent 40 μm. (b) Example of contralateral eye– and ipsilateral eye–driven calcium responses of the neurons shown in a that express high (neuron 1) or low (neuron 2) levels of mCherry–miR-132 sponge. Pink shaded area indicates period with visual stimulus. Calculated ODIs were 0.73 (neuron 1) and 0.55 (neuron 2). (c) ODI values (ODI = (contralateral – ipsilateral) / (contralateral + ipsilateral); mean ± s.e.m.) derived from peak visual responses obtained by two-photon calcium imaging in mice injected with mCherry–miR-132 sponge–expressing lentivirus. Black bars indicate mice subjected to 4 d of monocular deprivation and light gray bars indicate mice that were not subjected to monocular deprivation (miR-132 sponge non–monocular deprivation, five mice, 290 neurons; miR-132 sponge monocular deprivation, four mice, 232 neurons; control non–monocular deprivation; three mice, 120 neurons; control monocular deprivation, three mice, 177 neurons). The ODI did not shift following monocular deprivation in mice that were injected with miR-132 sponge, but not control, virus. A significantly larger ocular dominance shift was seen in control monocularly deprived mice than in any of the other conditions (**P < 0.01, Mann-Whitney test comparing neurons; P < 0.05 treating each mouse as a single datum).