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If the in vivo effects of anaesthesia are mediated through a specific receptor system, then a relationship could exist between the regional changes in brain metabolism caused by a particular agent and the underlying regional distribution of the specific receptors affected by that agent. Positron emission tomography data from volunteers studied while unconscious during propofol (n=8) or isoflurane (n=5) anaesthesia were used retrospectively to explore for evidence of relationships between regional anaesthetic effects on brain glucose metabolism and known (ex vivo) regional distribution patterns of human receptor binding sites. The regional metabolic reductions caused by propofol differed significantly from those of isoflurane. Propofol’s reductions negatively correlated most significantly with the regional distribution of [3H]diazepam and [3H]flunitrazepam (benzodiazepine) binding site densities (r=–0.86, P<0.0005; r=–0.79, P<0.005, respectively) and less strongly with [3H]naloxone (opioid) binding density (r=–0.69, P<0.05). Isoflurane’s reductions positively correlated only with muscarinic (acetylcholine) binding density (r=0.85, P<0.05). These findings are consistent with the hypothesis that some of propofol’s in vivo anaesthetic effects may be mediated through a GABAergic mechanism and suggest some of isoflurane’s in vivo effects might involve antagonism of central acetylcholine functioning.