Glutamate and GABA imbalance following traumatic brain injury

Curr Neurol Neurosci Rep. 2015 May;15(5):27. doi: 10.1007/s11910-015-0545-1.


Traumatic brain injury (TBI) leads to multiple short- and long-term changes in neuronal circuits that ultimately conclude with an imbalance of cortical excitation and inhibition. Changes in neurotransmitter concentrations, receptor populations, and specific cell survival are important contributing factors. Many of these changes occur gradually, which may explain the vulnerability of the brain to multiple mild impacts, alterations in neuroplasticity, and delays in the presentation of posttraumatic epilepsy. In this review, we provide an overview of normal glutamate and GABA homeostasis and describe acute, subacute, and chronic changes that follow injury. We conclude by highlighting opportunities for therapeutic interventions in this paradigm.

Publication types

  • Research Support, N.I.H., Extramural
  • Review

MeSH terms

  • Animals
  • Brain Injuries / complications
  • Brain Injuries / metabolism*
  • Brain Injuries / pathology
  • Epilepsy / etiology
  • Glutamic Acid / metabolism*
  • Homeostasis / physiology
  • Humans
  • Receptors, GABA / metabolism
  • Receptors, Glutamate / metabolism
  • gamma-Aminobutyric Acid / metabolism*


  • Receptors, GABA
  • Receptors, Glutamate
  • Glutamic Acid
  • gamma-Aminobutyric Acid