 Xenon interacts with many different receptors and ion channels and like many theoretically multi @-@ modal inhalation anesthetics these interactions are likely complementary . Xenon is a high @-@ affinity glycine @-@ site NMDA receptor antagonist . However , xenon distinguishes itself from other clinically used NMDA receptor antagonists in its lack of neurotoxicity and its ability to inhibit the neurotoxicity of ketamine and nitrous oxide . Unlike ketamine and nitrous oxide , xenon does not stimulate a dopamine efflux in the nucleus accumbens . Like nitrous oxide and cyclopropane , xenon activates the two @-@ pore domain potassium channel TREK @-@ 1 . A related channel TASK @-@ 3 also implicated in inhalational anesthetic actions is insensitive to xenon . Xenon inhibits nicotinic acetylcholine α4β2 receptors which contribute to spinally mediated analgesia . Xenon is an effective inhibitor of plasma membrane Ca2 + ATPase . Xenon inhibits Ca2 + ATPase by binding to a hydrophobic pore within the enzyme and preventing the enzyme from assuming active conformations . 
