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Differential actions of ethanol and trichloroethanol at sites in the M3 and M4 domains of the NMDA receptor GluN2A (NR2A) subunit

Background and purpose:  Alcohol produces its behavioural effects in part due to inhibition of N‐methyl‐d‐aspartate (NMDA) receptors in the CNS. Previous studies have identified amino acid residues in membrane‐associated domains 3 (M3) and 4 (M4) of the NMDA receptor that influence ethanol sensitivity. In addition, in other alcohol‐sensitive ion channels, sedative‐hypnotic agents have in some cases been shown to act at sites distinct from the sites of ethanol action. In this study, we compared the influence of mutations at these sites on sensitivity to ethanol and trichloroethanol, a sedative‐hypnotic agent that is a structural analogue of ethanol.