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Related Experiment Videos

Isoflurane blocks synaptic plasticity in the mouse hippocampus.

W Simon1, G Hapfelmeier, E Kochs

  • 1Max-Planck-Institute of Psychiatry, Munich, Germany.

Anesthesiology
|July 24, 2001
PubMed
Summary

Isoflurane anesthesia impairs synaptic plasticity, preventing long-term potentiation (LTP) and long-term depression (LTD) in juvenile and adult mouse hippocampus. This effect is reversible and linked to gamma-aminobutyric acid type A (GABA_A) receptors, potentially explaining cognitive deficits post-anesthesia.

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Area of Science:

  • Neuroscience
  • Anesthesiology
  • Synaptic Plasticity

Background:

  • The volatile anesthetic isoflurane is known to depress glutamatergic transmission.
  • Synaptic plasticity, including long-term potentiation (LTP) and long-term depression (LTD), relies on glutamate receptor activation.
  • Investigating isoflurane's impact on LTP and LTD in the hippocampus is crucial for understanding its neurological effects.

Purpose of the Study:

  • To investigate the effects of isoflurane on the induction of LTP and LTD in hippocampal slices from juvenile and adult mice.
  • To explore the role of gamma-aminobutyric acid type A (GABA_A) receptors in mediating isoflurane's effects on synaptic plasticity.

Main Methods:

  • Extracellular field excitatory postsynaptic potentials (fEPSPs) and intracellular excitatory postsynaptic currents (EPSCs) were recorded from CA1 hippocampal neurons.

Related Experiment Videos

  • Synaptic transmission was stimulated via the Schaffer collateral-commissural pathway.
  • Clinically relevant concentrations of isoflurane (0.2-0.3 mM) were applied, and GABA_A receptor antagonists were used.

    • Main Results:

    • Isoflurane significantly depressed fEPSPs and EPSCs in both juvenile and adult mouse hippocampus slices.
    • Tetanic stimulation failed to induce LTP in the presence of isoflurane, though the effect was reversible.
    • Low-frequency stimulation failed to induce LTD when isoflurane was present.

    Conclusions:

    • Isoflurane inhibits the induction of both LTP and LTD in the hippocampus, suggesting a broad impact on synaptic plasticity.
    • The prevention of isoflurane's effects by a GABA_A receptor antagonist indicates a critical role for these receptors.
    • Enhanced GABAergic inhibition by isoflurane may prevent necessary postsynaptic depolarization, potentially underlying post-anesthetic cognitive impairment.