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Related Experiment Videos

Acute decrease in net glutamate uptake during energy deprivation.

D Jabaudon1, M Scanziani, B H Gähwiler

  • 1Brain Research Institute, University of Zurich, CH-8057 Zurich, Switzerland.

Proceedings of the National Academy of Sciences of the United States of America
|May 11, 2000
PubMed
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During cerebral ischemia, reduced glutamate uptake and increased release cause excitotoxicity. This study reveals early glutamate accumulation mechanisms, crucial for understanding neuronal death during stroke.

Area of Science:

  • Neuroscience
  • Cellular Biology
  • Pathophysiology

Background:

  • Extracellular glutamate concentration ([glu](o)) increases during cerebral ischemia, potentially causing delayed neuronal death.
  • The precise mechanisms driving glutamate accumulation in ischemia are not fully understood.

Purpose of the Study:

  • To investigate the sources of glutamate release during in vitro ischemia using CA3 pyramidal neurons as a glutamate sensor.
  • To elucidate the roles of glutamate transporters and vesicular release in glutamate accumulation during energy deprivation.

Main Methods:

  • Utilized N-methyl-D-aspartate receptors on CA3 pyramidal neurons to monitor extracellular glutamate in real-time.
  • Employed glutamate and L-trans-pyrrolidine-2,4-dicarboxylic acid (tPDC) as substrates and DL-threo-beta-benzyloxyaspartate (TBOA) to inhibit glutamate transporters.

Related Experiment Videos

  • Applied an in vitro model of cerebral ischemia to induce energy deprivation.

    • Main Results:

    • Energy deprivation rapidly decreased net glutamate uptake within 2-3 minutes.
    • Reverse glutamate transport contributed significantly (up to 50%) to glutamate accumulation.
    • Action potential-independent vesicular release accounted for approximately 50% of the increase in extracellular glutamate, particularly after transporter inhibition.

    Conclusions:

    • Significant extracellular glutamate rise occurs within minutes of energy deprivation.
    • Both reduced glutamate uptake and increased vesicular/nonvesicular release contribute to excitotoxicity during early ischemia.