 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 . 
 Xenon interacts with many different receptors and ion channels and like many theoretically multi @-@ modal inhalation anesthetics these interactions <a href='drop_aux' title='1'><mark>are</mark></a>likely complementary . Xenon <a href='drop_aux' title='2'><mark>is</mark></a>a high @-@ affinity glycine @-@ site NMDA receptor antagonist . However , xenon <a href='uninflect' title='3'><mark>distinguishes</mark></a> 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 <a href='negative_concord' title='4'><mark>ketamine</mark></a> and nitrous oxide , xenon <a href='uninflect' title='5'><mark>does</mark></a> not stimulate <a href='None' title='6'><mark>a</mark></a>dopamine <a href='negative_concord' title='7'><mark>efflux</mark></a> in the nucleus accumbens . Like nitrous oxide and cyclopropane , xenon <a href='uninflect' title='8'><mark>activates</mark></a> the two @-@ pore domain potassium channel TREK @-@ 1 . A related channel TASK @-@ 3 also implicated in inhalational anesthetic actions <a href='drop_aux' title='9'><mark>is</mark></a>insensitive to xenon . Xenon <a href='uninflect' title='10'><mark>inhibits</mark></a> nicotinic acetylcholine α4β2 receptors which contribute to spinally mediated analgesia . Xenon <a href='drop_aux' title='11'><mark>is</mark></a>an effective inhibitor of plasma membrane Ca2 + ATPase . Xenon <a href='uninflect' title='12'><mark>inhibits</mark></a> Ca2 + ATPase by binding to a hydrophobic pore within the enzyme and preventing the enzyme from assuming active conformations . 
Xenon interacts witt many different receptors and ion channels and like many theoretically multi @-@ modal inhalation anesthetics dese interactions likely complementary . Xenon a high @-@ affinity glycine @-@ site NMDA receptor antagonist . However , xenon distinguish itself from other clinically used NMDA receptor antagonists in its lack of neurotoxicity and its ability to inhibit da neurotoxicity of ketamine and nitrous oxide . Unlike no ketamine and nitrous oxide , xenon do not stimulate dopamine no efflux in tdanucleus accumbens . Like nitrous oxide and cyclopropane , xenon activate the two @-@ pore domain potassium channel TREK @-@ 1 . A related channel TASK @-@ 3 also implicated in inhalational anesthetic actions insensitive to xenon . Xenon inhibit nicotinic acetylcholine α4β2 receptors which contribute to spinally mediated analgesia . Xenon an effective inhibitor of plasma membrane Ca2 + ATPase . Xenon inhibit Ca2 + ATPase by binding to a hydrophobic pore within the enzyme and preventing thdanzyme from assuming active conformations .