title: Glutamate and GABA imbalance following traumatic brain injury.
abstract: 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.
authors: Division Epilepsy, Department of Neurology, Boston Children's Hospital and Harvard Medical School, 300 Longwood Ave, Boston, MA, 02115, USA, Rejean.guerriero@childrens.harvard.edu.
authors: Réjean M
authors: RM
authors: Guerriero
authors: Christopher C
authors: CC
authors: Giza
authors: Alexander
authors: A
authors: Rotenberg
mesh_terms: D000818:Animals; D001930:Brain Injuries / Q000150:complications / Q000378:metabolism* / Q000473:pathology; D004827:Epilepsy / Q000209:etiology; D018698:Glutamic Acid / Q000378:metabolism*; D006706:Homeostasis / Q000502:physiology; D006801:Humans; D018079:Receptors, GABA / Q000378:metabolism; D017470:Receptors, Glutamate / Q000378:metabolism; D005680:gamma-Aminobutyric Acid / Q000378:metabolism*
chemical_list: D018079:Receptors, GABA; D017470:Receptors, Glutamate; D018698:Glutamic Acid; D005680:gamma-Aminobutyric Acid