2ZD1 Whole-cell patch-clamp recordings were used to investigate the e ects of the anaesthetic Sa an on the electrophysiological properties of sympathetic preganglionic neurones (SPNs) in rat spinal cord slices. 2 Sa an (1 ± 54 mM) abolished or reduced the frequency of spontaneous action potential ®ring and abolished spontaneous, sub-threshold membrane potential oscillations. Sa an caused dose-dependent decreases in input resistance and depending upon the initial resting membrane potential, either a depolarization, a hyperpolarization or no change in membrane potential. 3 Responses to Sa an were blocked by the GABA A receptor antagonists bicuculline (5 ± 20 mM) and picrotoxin (20 mM), but not by the glycine receptor antagonist strychnine (20 mM) indicating that they were mediated by GABA A receptors. 4 Changes in the properties of SPN action potentials were also observed. In the presence of Sa an the amplitude and duration of the action potential after-hyperpolarization were reduced and larger depolarizations were required in order to evoke trains of action potentials. 5 To examine the e ects of Sa an on electrotonic coupling between SPNs, experiments were performed with the Na + channel blocker QX-314 in the intracellular solution and antidromic oscillations were evoked by ventral root stimulation. Sa an failed to abolish antidromic oscillations, but reduced their amplitude and duration. This indicates that the abolition of spontaneous membrane potential oscillations was not a direct e ect on the coupling between SPNs, but was a result of the abolition of spontaneous activity by Sa an. 6 The responses to Sa an occurred within the plasma concentration range of Sa an during anaesthesia, suggesting that the electrophysiological properties of SPNs may be altered during anaesthesia with Sa an. This would be expected to lead to changes in sympathetic tone and in the integration of sympathetic output.