One of the most amazing aspects of stroke is how survivors often exhibit partial recovery from their deficits. This occurs presumably because of remapping of lost capabilities to functionally related brain areas in both hemispheres. Several functional imaging studies in humans and rats suggest that remapping in the contralateral (uninjured) cortex might represent a transient stage of compensatory plasticity, until more permanent forms of circuit rewiring in peri-infarct cortex can take over. Some postmortem studies in fixed tissue have suggested that cortical lesions (including stroke) trigger extensive dendritic plasticity in the contralateral hemisphere, but this remains controversial (as others could not replicate the results) and no mechanism has yet been established as to how this remapping might occur. I used longitudinal in vivo two-photon microscopy in the contralateral homotopic cortex to record changes in dendritic spines in apical tufts of layer 5 (L5) pyramidal neurons in adult thy1 GFP-M mice before and after stroke. In addition, I used intrinsic optical signal (IOS) imaging to investigate whether sensory functions that were lost after stroke remapped to the contralateral homotopic cortex. Strokes were induced by either rose Bengal photothrombosis or unilateral middle cerebral artery occlusion, both of which produced cortical infarcts that spanned the forelimb region of primary somatosensory cortex. For spine dynamics, mice were imaged longitudinally every 4 days for a baseline period before the stroke, and for up to one month thereafter. For IOS imaging, I mapped the sensory responses to ipsi- and contralateral forelimb and hindlimb stimulation at baseline conditions and then again every few days at regular intervals for up to 28 days after stroke in both adult and juvenile mice. The peri-infarct region showed significant remapping after stimulation of a whisker bundle after stroke, and stimulation of the contralateral forepaw always produced a strong intrinsic signal, but stimulation of the ipsilateral forepaw never resulted in a detectable signal in the spared homotopic cortex opposite to the side of the stroke. Similarly, I could not detect de novo growth or branching of dendrites or any changes in the density or turnover of spines after stroke. Thus, the contralesional cortex does not show evidence of structural plasticity after stroke, at least at the level of apical dendritic tufts of L5 neurons, or of functional remapping as detectable with IOS. This suggests that, at least in mice, the peri-infarct cortex plays the dominant role in post-ischemic reparative plasticity.