The loss of a sensory input leads to reorganization of neuronal networks in remaining sensory cortices, which results in functional improvements. This shows remarkable adaptability of the mammalian brain. It remains elusive whether a traumatic brain injury (TBI) in a sensory cortex results in similar functional reorganization in spared sensory networks. We herein investigated global alterations in neuronal activity maps in the mouse brain subjected to a TBI in the visual cortex and delved into the underlying cellular mechanisms. Our data shows substantial differences in brain activity maps 2-3 months after TBI. Interestingly, the unbiased brain-wide analysis revealed an increased number of active neurons in brain regions that encode olfactory information, including the olfactory bulb (OB) and olfactory cortex, and thus suggest remodeling of the underlying circuitry. Unlike most adult mammalian brains, the OB retains the ability to integrate new neurons throughout an animal's life. We demonstrate a considerable increase in the number of new neurons in OB circuits in the TBI brain, together with higher GABA and gephyrin levels. In addition, trans-synaptic tracing reveals increased cortical feedback. Noteworthy, both modifications to the OB circuitry are predicted to result in improved performance in olfactory behavior tests, which we confirmed in odor sensitivity task. Large-scale multielectrode recordings further elucidate circuit physiology. This work offers valuable contributions to the field, shedding light on the extended consequences of a focal brain injury, eliciting adaptive mechanisms in remote brain networks. Moreover, it suggests that adult olfactory neurogenesis may be implicated in sensory compensation.