Cellular and synaptic actions of general anaesthetics

Abstract

1. This paper briefly reviews mechanisms by which such widely-used volatile anaesthetics as halothane and isoflurane suppress neural function in the brain. 2. In general, anaesthetics tend to depress neuronal firing and excitatory synaptic transmission, and potentiate synaptic inhibition. 3. According to recent evidence, a particular important action of anaesthetics is to inactivate a variety of both voltage-dependent and agonist-triggered Ca-currents. 4. Activation of K outward currents and Na inward currents probably occurs only with higher doses of anaesthetics. 5. How anaesthetics interfere with Ca-channels remains largely a matter of speculation--though some evidence favours a Ca-mediated action, following Ca2+ release from internal stores, that may account also for potentiation of IPSPs by prolonging the opening of GABA-activated Cl- channels. 6. Whatever its precise underlying mechanism, a suppression of Ca-influx into pre-synaptic terminals could well account for the depression of excitatory synaptic transmission.