Related Experiment Video
Updated: Sep 20, 2026

Application of Dixon's Up-and-Down Design to Estimate the Minimum Alveolar Concentration of Sevoflurane in Rats with Refined Movement Classification
Published on: July 25, 2025
Inhaled anesthetics and immobility: mechanisms, mysteries, and minimum alveolar anesthetic concentration
James M Sonner1, Joseph F Antognini, Robert C Dutton
1*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.
Abstract:
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 amino 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., gamma-aminobutyric acid A, acetylcholine, potassium, 5-hydroxytryptamine-3, opioids, and alpha(2)-adrenergic), whereas other receptors/channels (e.g., glycine, N-methyl-D-aspartate, and sodium) remain credible candidates.
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