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Volatile and intravenous anesthetics decrease glutamate release from cortical brain slices during anoxia

P E Bickler1, L T Buck, J R Feiner

  • 1Department of Anesthesia, University of California School of Medicine, San Francisco 94143-0542, USA.

Anesthesiology
|December 1, 1995
PubMed
Summary
This summary is machine-generated.

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Certain anesthetics like halothane, enflurane, and sodium thiopental reduce the release of L-glutamate during hypoxic conditions, potentially protecting neurons. Propofol did not show this effect.

Area of Science:

  • Neuroscience
  • Anesthesiology
  • Neuroprotection

Background:

  • Extracellular L-glutamate accumulation during cerebral hypoxia/ischemia contributes to neuronal death.
  • Anesthetics are known to inhibit synaptic neurotransmitter release.
  • The effect of anesthetics on extrasynaptic glutamate release during hypoxia/ischemia is not well understood.

Purpose of the Study:

  • To investigate if different anesthetics decrease hypoxia-induced glutamate release from rat brain slices.
  • To determine the impact of clinical anesthetic concentrations on extrasynaptic glutamate release.

Main Methods:

  • Glutamate release from rat cortical brain slices was measured using fluorometry.
  • Measurements were taken under oxygenated, hypoxic, and anoxic conditions with various anesthetics (halothane, enflurane, propofol, sodium thiopental).

Related Experiment Videos

  • The source of glutamate release was identified using calcium channel blockers and calcium-free medium.

    • Main Results:

    • Hypoxia/anoxia significantly increased glutamate release compared to KCl depolarization.
    • Hypoxia/anoxia-induced glutamate release was likely due to reversed uptake mechanisms, not synaptic voltage-gated calcium channels.
    • Halothane, enflurane, and sodium thiopental reduced hypoxia-evoked glutamate release by 50-70% (P < 0.05).
    • Propofol did not significantly alter hypoxia-evoked glutamate release.

    Conclusions:

    • Halothane, enflurane, and sodium thiopental decrease extrasynaptic L-glutamate release during hypoxic stress at clinical concentrations.
    • Propofol does not exhibit this effect on extrasynaptic glutamate release.
    • These findings suggest a potential neuroprotective mechanism for certain anesthetics against hypoxic neuronal injury.