Prolonged reduction in blood flow leads to stroke, a devastating neurological insult leading cause of adult disability worldwide. One of the early features of stroke is the disruption of neuronal activity that results from the reduction of metabolic supply. Changes in oscillatory brain patterns have been observed in several neurological disorders, including stroke. Evoked neural oscillations in the gamma range have recently shown the ability to restore and maintain intrinsic homeostatic processes in the brain. However, the causal relationship between stimulation and restoration of function is not well understood. We aimed to determine the mechanisms behind the observed neuroprotective effects following optogenetic stimulation at 40 Hz by characterising electrophysiology and genomic profiling of inhibitory neurons. We used optogenetic stimulation together with laser speckle imaging, in vivo electrophysiology, and RNA sequencing in an awake photothrombotic stroke mouse model, to investigate the effects of entrained gamma modulation in the acute phase after stroke.We show that optogenetic stimulation at 40 Hz drives activation of inhibitory neurons specifically. We found that following stroke induction in the motor area (M1), 40 Hz stimulation enhances interregional communication between M1 and the posterior temporal area (PTA), and interestingly this is still present 24 hours after stimulation. Cross-correlogram analysis indicates that optogenetic stimulation of inhibitory neurons in the gamma range leads to an increase in functional synaptic plasticity observed 24 hours after stroke induction. Our results suggest that modulation of cortical oscillatory dynamics may serve as a target for neuroprotection after stroke by modulating synaptic connections.