TY - JOUR
T1 - Glutamate and GABA Imbalance Following Traumatic Brain Injury
AU - Guerriero, Réjean M.
AU - Giza, Christopher C.
AU - Rotenberg, Alexander
N1 - Funding Information:
Christopher C. Giza has received one-time consultancy fees from Alcobra and Pearson TLC. Dr. Giza has also received grants from the NCAA-DOD, NIH/NINDS, Joseph Drown Foundation, Today’s and Tomorrow’s Children Fund, UCLA Brain Injury Research Center, the UCLA Steve Tisch BrainSPORT Program, speaker honoraria from multiple academic institutions, royalties from Blackwell Publishing, payment for development of educational presentations from the Medical Education Speakers Bureau, and paid travel accommodations from the NCAA, USSF, MLS, and the California State Athletic Commission.
Funding Information:
Alexander Rotenberg declares a pending award related to TBI and posttraumatic loss of GABAergic cortical inhibition (NIH NINDS 1R01NS088583). Dr. Rotenberg is also supported by NIH, Department of Defense, CURE, and the Harvard Translational Research Program.
Publisher Copyright:
© 2015, Springer Science+Business Media New York.
PY - 2015/5
Y1 - 2015/5
N2 - 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.
AB - 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.
KW - Glutamate transporter
KW - NMDA receptor
KW - Parvalbumin interneuron
KW - Posttraumatic epilepsy
UR - http://www.scopus.com/inward/record.url?scp=84925307887&partnerID=8YFLogxK
U2 - 10.1007/s11910-015-0545-1
DO - 10.1007/s11910-015-0545-1
M3 - Review article
C2 - 25796572
AN - SCOPUS:84925307887
SN - 1528-4042
VL - 15
JO - Current Neurology and Neuroscience Reports
JF - Current Neurology and Neuroscience Reports
IS - 5
ER -