Traumatic brain injury (TBI) is the first cause of disability and death in Europe among children. Tremendous clinical and pre-clinical efforts have been undertaken to understand the acute, life-threatening events occurring right after severe TBI. TBI also causes significant complications and morbidity weeks, months or even years after the initial lesion. Memory and sensorimotor dysfunctions following TBI are not only caused by local destruction of brain tissue and but also by alterations in remote brain areas including contralateral sensorimotor cortex and hippocampus. The cellular and molecular mechanisms underlying the long-term alterations of remote brain areas after TBI are still poorly understood. Astrocytic coverage of synapses has been shown to be critical for efficiency of synaptic transmission by improving neurotransmitter clearance and ion homeostasis, limiting spillover of glutamate from synapses in the healthy brain. How astrocytic function is compromised and recovers after TBI is largely unknown. Astrocytic Aquaporin 4 (AQP4) water channels are thought to play a role in synaptic function and plasticity by regulating the extracellular space (ECS) in the healthy brain. After brain injury, when astrocytes become reactive, expression of AQP4-protein is markedly altered in a sustained way. The consequences of TBI-induced alterations in AQP4 expression for ECS are unknown. It is well known that physical therapy during the recovery from TBI can significantly improve the clinical outcome. The brain correlates and mechanisms of improved rehabilitation are poorly understood.