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Objective Reduction in neuronal activity in remote brain regions after stroke is likely caused by a disruption of afferent excitatory input originating from distant infarcted areas.Environmentally induced neuroplasticity has been shown to be effective in reducing impairment in many experimental models of brain injury and neurodegeneration.The current study sought to investigate the potential of enriched environment (EE) in resolving hippocampal diaschisis following experimental stroke and in reversing post stroke spatial memory deficits.Methods Stroke was induced by distal middle cerebral artery occlusion (dMCAO) in rats.Neuronal activation induced by spatial task was mapped by immediate early gene Fos and neuronal projections by anterograde tracer BDA.Memory function was determined by the Barnes maze test.Results Although neuronal loss and microglia activation were restricted to the parietal cortex following dMCAO, a region-specific reduction in neuronal activation was observed in the hippocampus following pharmacological challenge with sulpiride.Housing in the EE not only reduced post stroke impairment in spatial learning and memory, increased hippocampal neurogenesis, but also restored hippocampal activation during memory task.Neuronal tracing indicated that the parietal cortex projected extensively to the parahippocampal region.Exposure to EE also restored the Fos expression in the entorhinal and perirhinal cortices ipsilateral to infarct, suggesting that hippocampal hypoactivation could be an indirect consequence of altered cortical inputs to the parahippocampal region that acts like a key gateway for information exchange between cortex and hippocampus.Importantly, EE reduced neuronal loss in the peri-infarct area of the parietal cortex, suggesting that the beneficial effects of EE on neuronal activity and memory function was likely due to a partial preservation of the cortical inputs to the parahippocampal area.Conclusion Our findings point to the potential of EE in resolving hippocampal diaschisis via plasticity and neuorprotection mechanisms that affect hippocampal-cortical networks and contribute to brain remodeling.