Prolonged deficit of low gamma oscillations in the peri-infarct cortex of mice after stroke.

Days and weeks after an ischemic stroke, the peri-infarct area adjacent to the necrotic tissue exhibits very intense synaptic reorganization aimed at regaining lost functions. In order to enhance functional recovery, it is important to understand the mechanisms supporting neural repair and neuroplasticity in the cortex surrounding the lesion. Brain oscillations of the local field potential (LFP) are rhythmic fluctuations of neuronal excitability that synchronize neuronal activity to organize information processing and plasticity. Although the oscillatory activity of the brain has been probed after stroke in both animals and humans using electroencephalography (EEG), the latter is ineffective to precisely map the oscillatory changes in the peri-infarct zone where synaptic plasticity potential is high. Here, we worked on the hypothesis that the brain oscillatory system is altered in the surviving peri-infarct cortex, which may slow down the functional repair and reduce the recovery. In order to document the relevance of this hypothesis, oscillatory power was measured at various distances from the necrotic core at 7 and 21 days after a permanent cortical ischemia induced in mice. Delta and theta oscillations remained at a normal power in the peri-infarct cortex, in contrast to low gamma oscillations that displayed a gradual decrease, when approaching the border of the lesion. A broadband increase of power was also observed in the homotopic contralateral sites. Thus, the proximal peri-infarct cortex could become a target of therapeutic interventions applied to correct the oscillatory regimen in order to boost post-stroke functional recovery.