The role of glutamate receptors in traumatic brain injury: implications for postsynaptic density in pathophysiology

Brain Res Bull. 2011 Jul 15;85(6):313-20. doi: 10.1016/j.brainresbull.2011.05.004. Epub 2011 May 13.


Traumatic brain injury (TBI) is the major cause of death and disability, and the incidence of TBI continues to increase rapidly. In recent years, increasing attention has been paid to an important structure at the postsynaptic membrane: the postsynaptic density (PSD). Glutamate receptors, as major components of the PSD, are highly responsive to alterations in the glutamate concentration at excitatory synapses and activate intracellular signal transduction via calcium and other second messengers following TBI. PSD scaffold proteins (PSD-95, Homer, and Shank), which anchor glutamate receptors and form a network structure, also have potential effects on these downstream signaling pathways. The changes in the function and structure of these major PSD proteins are also induced by TBI, indicating that there is a more complicated mechanism associated with PSD proteins in the pathophysiological process of TBI.

Publication types

  • Research Support, Non-U.S. Gov't
  • Review

MeSH terms

  • Brain Injuries / metabolism
  • Brain Injuries / pathology
  • Brain Injuries / physiopathology*
  • Glutamic Acid / metabolism
  • Humans
  • Nerve Tissue Proteins / metabolism
  • Post-Synaptic Density / metabolism*
  • Receptors, Glutamate / metabolism*
  • Signal Transduction / physiology


  • Nerve Tissue Proteins
  • Receptors, Glutamate
  • postsynaptic density proteins
  • Glutamic Acid