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*Department of Anesthesia and Perioperative Care, University of California, San Francisco, California;
Department of Anesthesiology, University of California, Davis, California;
Columbia University, New York, New York;
University of Texas, Austin, Texas;
||University of Pittsburgh, Pittsburgh, Pennsylvania;
¶Stanford University, Palo Alto, California;
#University of Toronto, Toronto, Canada;
**Department of Anaesthesia, Harvard Medical School, Cambridge, Massachusetts; and
Garvan Institute of Medical Research, Darlinghurst, Australia
Address correspondence and reprint requests to James M. Sonner, MD, Department of Anesthesia, S-455, University of California, San Francisco, CA 94143-0464. Address e-mail to sonnerj{at}anesthesia ucsf.edu.
Studies using molecular modeling, genetic engineering, neurophysiology/pharmacology, and whole animals have advanced our understanding of where and how inhaled anesthetics act to produce immobility (minimum alveolar anesthetic concentration; MAC) by actions on the spinal cord. Numerous ligand- and voltage-gated channels might plausibly mediate MAC, and specific animo acid sites in certain receptors present likely candidates for mediation. However, in vivo studies to date suggest that several channels or receptors may not be mediators (e.g., 
-aminobutyric acid A, acetylcholine, potassium, 5-hydroxytryptamine-3, opioids, and 
2-adrenergic), whereas other receptors/channels (e.g., glycine, N-methyl-D-aspartate, and sodium) remain credible candidates.
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M. Shiraishi and R. A. Harris Effects of Alcohols and Anesthetics on Recombinant Voltage-Gated Na+ Channels J. Pharmacol. Exp. Ther., June 1, 2004; 309(3): 987 - 994. [Abstract] [Full Text] [PDF]
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N. L. Harrison Knockin' on the Door of General Anesthetic Mechanisms: But Will U.S. Researchers Be Shut Out? Anesth. Analg., September 1, 2003; 97(3): 616 - 618. [Full Text] [PDF]
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