Glutamate excitotoxicity plays an important role in the development of secondary injuries
that occur following traumatic brain injury (TBI), and contributes significantly to expansion of
the total volume of injury. Acute increases in extracellular glutamate levels have been
detected in both experimental brain trauma models and in human patients, and can lead to
over-stimulation of glutamate receptors, resulting in a cascade of excitotoxic-related
mechanisms culminating in neuronal damage. These elevated levels of glutamate can be …