Halothane modulates NMDA and non-NMDA excitatory synaptic transmission in rat cortical neurons

Although general anesthetics may decrease neuronal excitation, their detailed effects on spontaneous excitatory postsynaptic currents (EPSCs) remain controversial. We investigated and compared the effects of halothane on N-methyl-D-asparate (NMDA) and non-NMDA receptor-mediated postsynaptic currents. Spontaneous synaptic currents were recorded by the patch clamp technique in cultured rat cortical neurons. They were isolated by specific pharmacological blocking agents and their electrophysiologic properties were examined. The frequency of NMDA EPSCs was preferentially decreased as compared with that of non-NMDA EPSCs at halothane 1.2 mM. The total net charge of EPSCs mediated by NMDA and non-NMDA receptors was depressed to 56% +/- 6% (mean +/- SD) and 71% +/- 7% of control by halothane 0.6 mM, and to 11% +/- 9% and 59% +/- 11% of control by halothane 1.2 mM, respectively. These results show that halothane causes decrease of excitatory synaptic activity, with NMDA EPSCs being more sensitive than non-NMDA EPSCs.