To solve the complex mechanisms during the recovery process, each element of neuronal and glial responses should be studied separately. Neuronal circuits damaged by TBI also start multiple programs for functional recovery and regeneration, such as synaptic plasticity, neurogenesis, gliogenesis, and axonal sprouting ( Schoch et al., 2012 Nudo, 2013). Many pathologic events occur after TBI, such as changes in cellular conditions like ionic balance, glucose metabolism and free radical generation ( Prins et al., 2013), together with morphologic changes including axonal degeneration and synapse elimination ( Park and Biederer, 2013). One of the causes of the failure is heterogeneity of pathophysiology. However, promising drugs which were effective in TBI models have all failed in clinical trials for human ( Xiong et al., 2013). Multiple animal models that replicate human TBI have been developed for better understanding of TBI pathophysiology and exploring therapeutic targets ( Xiong et al., 2013). It is important to propose new therapeutic strategies for the improvement of survival rate and reduction of disability, not only prevent TBI itself. Traumatic brain injury (TBI) is a major cause of death and disability in multiple countries and contributes to ∼30% of all injury deaths in the United States ( Taylor et al., 2017). Taken together, these findings suggest that postsynaptic changes occur in afferent elimination are NMDA dependent and imply that these NMDA-dependent events underlie synaptic remodeling of TBI. Also, these events could be blocked or delayed by NMDA receptor inhibition. These translocation events started after the loss of contacting presynaptic sites. Some of the postsynaptic sites initially located inside spines showed translocation toward dendritic shafts. Specifically, loss of presynaptic sites preceded loss of postsynaptic sites and spines. Afferent elimination can induce various events related to synapse remodeling and we could determine their temporal orders and find relationships between them. We focused on synapse remodeling which plays an important role in recovery from TBI and developed a new method, afferent elimination, for analyzing synapse remodeling after selective damage to presynaptic axons by mechanical transection in culture of mouse hippocampal neurons. To facilitate understanding of TBI pathophysiology, each element of neuronal and glial responses should be studied separately. However, heterogeneity of pathophysiology obstructs discovery of therapeutic targets. Multiple animal models have been developed to explore therapeutic targets for TBI. Traumatic brain injury (TBI) is one of the major causes of death and disability.
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