Halothane modulates NMDA and non-NMDA excitatory synaptic transmission in rat cortical neurons

J Anesth. 2005;19(1):66-72. doi: 10.1007/s00540-004-0285-x.

Abstract

Purpose: Although general anesthetics may decrease neuronal excitation, their detailed effects on spontaneous excitatory postsynaptic currents (EPSCs) remain controversial. We investigated and compared the effects of halothane on N-methyl-D-asparate (NMDA) and non-NMDA receptor-mediated postsynaptic currents.

Methods: Spontaneous synaptic currents were recorded by the patch clamp technique in cultured rat cortical neurons. They were isolated by specific pharmacological blocking agents and their electrophysiologic properties were examined.

Results: The frequency of NMDA EPSCs was preferentially decreased as compared with that of non-NMDA EPSCs at halothane 1.2 mM. The total net charge of EPSCs mediated by NMDA and non-NMDA receptors was depressed to 56% +/- 6% (mean +/- SD) and 71% +/- 7% of control by halothane 0.6 mM, and to 11% +/- 9% and 59% +/- 11% of control by halothane 1.2 mM, respectively.

Conclusion: These results show that halothane causes decrease of excitatory synaptic activity, with NMDA EPSCs being more sensitive than non-NMDA EPSCs.

MeSH terms

  • Algorithms
  • Anesthetics, Inhalation / pharmacology*
  • Animals
  • Cerebral Cortex / cytology*
  • Cerebral Cortex / drug effects
  • Electrophysiology
  • Excitatory Postsynaptic Potentials / drug effects*
  • Glutamates / physiology
  • Halothane / pharmacology*
  • Kinetics
  • Membrane Potentials / drug effects
  • Neurons / drug effects*
  • Patch-Clamp Techniques
  • Rats
  • Rats, Sprague-Dawley
  • Receptors, N-Methyl-D-Aspartate / drug effects*
  • Synaptic Transmission / drug effects*
  • gamma-Aminobutyric Acid / physiology

Substances

  • Anesthetics, Inhalation
  • Glutamates
  • Receptors, N-Methyl-D-Aspartate
  • gamma-Aminobutyric Acid
  • Halothane