Open AccessDoes Anesthetic Additivity Imply a Similar Molecular Mechanism of Anesthetic Action at N-Methyl-D-Aspartate Receptors?
Author(s) -
Robert J Brosnan,
Trung L. Pham
Publication year - 2011
Publication title -
anesthesia and analgesia/anesthesia and analgesia
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.404
H-Index - 201
eISSN - 1526-7598
pISSN - 0003-2999
DOI - 10.1213/ane.0b013e3182080599
Subject(s) - nmda receptor , isoflurane , anesthetic , pharmacology , ketamine , receptor , mechanism of action , medicine , glycine , biophysics , anesthesia , chemistry , biochemistry , in vitro , biology , amino acid
Isoflurane and carbon dioxide (CO(2)) negatively modulate N-methyl-d-aspartate (NMDA) receptors, but via different mechanisms. Isoflurane is a competitive antagonist at the NMDA receptor glycine binding site, whereas CO(2) inhibits NMDA receptor current through extracellular acidification. Isoflurane and CO(2) exhibit additive minimum alveolar concentration effects in rats, but we hypothesized that they would not additively inhibit NMDA receptor currents in vitro because they act at different molecular sites.