Nitrous oxide (laughing gas) facilitates excitability in rat hippocampal slices through gamma-aminobutyric acid A receptor-mediated disinhibition.

ALTHOUGH nitrous oxide is safe when administered by anesthesiologists, misuse may result in brain damage either via asphyxia or via direct effects resulting in vacuole formation in cingulate and retrosplenial cortices under normoxic conditions. The direct toxic effects of nitrous oxide raise the possibility that nitrous oxide toxicity results from excitatory effects of the drug. To determine how nitrous oxide affects neuronal excitability, we studied the actions of nitrous oxide on excitatory synaptic transmission and pyramidal neuron excitability in the CA1 region of rat hippocampal slices using a paired pulse stimulation paradigm and a range of stimulus intensities and intervals.