Action of isoflurane on the substantia gelatinosa neurons of the adult rat spinal cord

The effects of a clinically relevant concentration (1.5%, 1 rat minimum alveolar concentration) of isoflurane diminished dorsal root-evoked polysynaptic, but not monosynaptic excitatory postsynaptic currents. In contrast, isoflurane prolonged the decay phase of evoked and miniature gamma-aminobutyric acidA receptor-mediated inhibitory postsynaptic currents. This may be a possible mechanism for antinociception by isoflurane in the spinal cord.