Traumatic brain injury down-regulates glial glutamate transporter (GLT- 1 and GLAST) proteins in rat brain

Vemuganti L. Raghavendra Rao, Mustafa K. Başkaya, Aclan Doǧan, Jeffrey D. Rothstein, Robert J. Dempsey

Research output: Contribution to journalArticlepeer-review

185 Scopus citations


Excess activation of NMDA receptors is felt to participate in secondary neuronal damage after traumatic brain injury (TBI). Increased extracellular glutamate is active in this process and may result from either increased release or decreased reuptake. The two high-affinity sodium-dependent glial transporters [glutamate transporter 1 (GLT-1) and glutamate aspartate transporter (GLAST)] mediate the bulk of glutamate transport. We studied the protein levels of GLT-1 and GLAST in the brains of rats after controlled cortical impact-induced TBI. With use of subtype-specific antibodies, GLT-1 and GLAST proteins wee quantitated by immunoblotting in the ipsilateral and contralateral cortex at 2, 6, 24, 72, and 168 h after the injury. Sham- operated rats served as control. TBI resulted in a significant decrease in GLT-1 (by 20-45%, p < 0.05) and GLAST (by 30-50%; p < 0.05) protein levels between 6 and 72 h after the injury. D-[3H]Aspartate binding also decreased significantly (by 30-50%, p < 0.05) between 6 and 72 h after the injury. Decreased glial glutamate transporter function may contribute to the increased extracellular glutamate that may mediate the excitotoxic neuronal damage after TBI. This is a first report showing altered levels of glutamate transporter proteins after TBI.

Original languageEnglish (US)
Pages (from-to)2020-2027
Number of pages8
JournalJournal of neurochemistry
Issue number5
StatePublished - May 1998
Externally publishedYes


  • GLT-1
  • Glutamate
  • Transporters
  • Traumatic brain injury
  • Uptake

ASJC Scopus subject areas

  • Biochemistry
  • Cellular and Molecular Neuroscience


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