Glutamate Transporters: Molecular Mechanisms of Functional Alteration and Role in the Development of Excitotoxic Neuronal Injury

  • Davide Trotti
  • Niels C. Danbolt
  • Barbara Lodi Rizzini
  • Paola Bezzi
  • Daniela Rossi
  • Giorgio Racagni
  • Andrea Volterra
Part of the GWUMC Department of Biochemistry and Molecular Biology Annual Spring Symposia book series (GWUN)

Abstract

Glutamate uptake is essential to maintain resting extracellular glutamate ([Glu]0) ≤ 1 μM, a concentration not producing significant activation of excitatory aminoacid (EAA) receptors’. Thereby, sharp synaptic signalling takes place upon glutamate release, while receptor overstimulation leading to excitotoxic neuronal damage is avoided. Modulatory changes of glutamate uptake may affect fast excitatory transmission2, while impaired or reversed transport likely participates to the neuropathology of ischemia/reperfusion injury3 and amyotrophic lateral sclerosis4 (ALS).

Keywords

Arachidonic Acid Amyotrophic Lateral Sclerosis Glutamate Transporter Glutamate Uptake Glial Glutamate Transporter 
These keywords were added by machine and not by the authors. This process is experimental and the keywords may be updated as the learning algorithm improves.

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Copyright information

© Springer Science+Business Media New York 1996

Authors and Affiliations

  • Davide Trotti
    • 1
  • Niels C. Danbolt
    • 2
  • Barbara Lodi Rizzini
    • 1
  • Paola Bezzi
    • 1
  • Daniela Rossi
    • 1
  • Giorgio Racagni
    • 1
  • Andrea Volterra
    • 1
  1. 1.Center of Neuropharmacology, Institute of Pharmacological SciencesUniversity of MilanItaly
  2. 2.Department of Anatomy, Institute of Basic Medical SciencesUniversity of OsloOsloNorway

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