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. 2023 Jul 14;17:1225191. doi: 10.3389/fnins.2023.1225191

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Copyright © 2023 McGuigan, Marie, O'Bryan, Flores, Evered, Silbert and Scott.

This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) and the copyright owner(s) are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.

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Effects of xenon on synaptic transmission and neuronal excitability. Xenon influences a number of membrane bound proteins present in the presynaptic terminal that regulate neurotransmitter release. Inhibition of the nicotinic acetylcholine receptor (nAChR) would prevent depolarization and reduce the probability of neurotransmitter release. Inhibition of presynaptic NMDAR and potentiation of GABAR would also reduce probability of neurotransmitter release. In contrast, inhibition of plasmalemmal calcium ATPase (PMCA) would promote release. Xenon reduces ionic current through NMDAR and AMPAR at the postsynaptic terminal. Potentiation of hyperpolarizing ionic currents through potassium channels (K2P, KATP) and inhibition of the depolarizing ionic current through the hyperpolarization activated cyclic nucleotide channel 2 (HCN2) reduce neuronal membrane excitability. Green Xe = xenon increases ionic current, Red Xe = xenon reduces ionic current. Created with BioRender.com.