[Molecular and cellular actions of inhalation anesthetics]

The cellular and molecular basis of inhalational anaesthesia is still unknown. Recent biochemical, neurophysiological and pharmacological interest has focussed on membrane proteins in the neuron, the smallest functional entity in the brain. In this review, the effects on ion transport and ion channels potentially relevant to anaesthesia are analysed with reference to the most extensively investigated volatile anaesthetics ether, chloroform, halothane, methoxyflurane, isoflurane, and enflurane. Synaptic transmission proved a major target of all the volatile substances tested so far. Their inhibitory effect seems to be due to an alteration in the Ca(2+)-dependent stimulus-secretion coupling within the presynaptic nerve endings. In contrast, the phosphatidylinositol pathway proved relatively insensitive. In the postsynaptic membrane, receptor-operated ion channels, K+ and Cl- channels are considered possible targets for anaesthetic vapours. Likewise, guanine nucleotide-binding proteins, so-called G proteins, are promising candidates for future research. So far, only limited data exist on the effects of anaesthetics on non-neuronal cellular components of the CNS, e.g. glial cells. In view of the rapidly increasing number of potential target mechanisms, the future challenge of biologically oriented anaesthesia research will be to puzzle out those mechanisms most relevant to the still mysterious state of anaesthesia.