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Nitrous oxide-induced enhancement of gamma-aminobutyric acidA-mediated chloride currents in acutely dissociated hippocampal neurons


, : Nitrous oxide-induced enhancement of gamma-aminobutyric acidA-mediated chloride currents in acutely dissociated hippocampal neurons. Anesthesiology 88(2): 473-480

Background: Because the synaptic inhibition in the human brain is largely mediated by gamma-aminobutyric acid (GABA), the GABA receptor is of primary interest for the study of the working mechanism of general anesthetics. This article examines the interaction between this type of ion channel and nitrous oxide (N2O). Methods: Patch clamp recording techniques were applied to investigate the effects of N2O on GABAA receptor channels in a whole-cell configuration at room temperature. Acutely dissociated rat hippocampal cells from the CA1 region were used. Rapid application of the agonist muscimol and anesthetics (N2O, pentobarbital, and ethanol) was accomplished using a Y tube application system. Peak chloride (Cl-) currents were measured. Results: Short-term application of muscimol (5-30 muM) with dissolved N2O (80%, apprxeq 22.5 mM) increased the Cl- current (apprxeq 140%) compared with muscimol alone. This effect is comparable with results the authors obtained with ethanol (800 mM) and pentobarbital (100 muM). Prolonged exposure (9 min) to N2O further increased Cl- Currents by an additional 50%. Concentrations of N2O lower than 12 mM did not show an enhancement of this current, whereas application of N2O alone did not result in any Cl- conductance. Conclusions: These results indicate that NO can enhance GABA. channel-mediated Cl- currents by modulating the effect of the specific GABAA agonist; it is not active by itself.

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PMID: 9477068


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