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Traumatic brain injury is primarily caused by deformations of the brain tissue due to mechanical trauma, followed by rapid release of glutamate and subsequent excitotoxicity (secondary damage). Additionally, the early phase of secondary injury has been found to cause loss of dendritic spines and formation of varicosities along dendrites and axons. Our lab’s recent findings using an in vitro model of NMDA-induced injury demonstrate that cytosolic PSD-95 interactor protein (cypin) promotes functional recovery following TBI by regulating dendritic spine loss and recovery. We also screened a number of small molecules for activation of cypin and found that compounds that increase cypin's guanine deaminase activity promote increases in higher order dendrites in vitro. The question that still remains to be answered is whether manipulation of cypin promotes functional recovery of neurons following TBI in vitro. We will use primary cultures of hippocampal and cortical neurons as a model system for our electrophysiological experiments aiming to provide evidence for the role of cypin in functional recovery of neurons following TBI.
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