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From the *Department of Anesthesia and Perioperative Care, University of California, San Francisco, California; Department of Anesthesia and Critical Care, Massachusetts General Hospital and Harvard Medical School, Boston, Massachusetts; Department of Anesthesia, Columbia University, New York City, New York; and Departments of Anesthesiology and Pharmacology, Weill Cornell Medical College, New York City, New York.
Address correspondence and reprint requests to Dr. Edmond I Eger II, Department of Anesthesia, S-455, University of CA, San Francisco, CA 94143-0464. Address e-mail to egere{at}anesthesia.ucsf.edu.
A paradox arises from present information concerning the mechanism(s) by which inhaled anesthetics produce immobility in the face of noxious stimulation. Several findings, such as additivity, suggest a common site at which inhaled anesthetics act to produce immobility. However, two decades of focused investigation have not identified a ligand- or voltage-gated channel that alone is sufficient to mediate immobility. Indeed, most putative targets provide minimal or no mediation. For example, opioid, 5-HT3, 
-aminobutyric acid type A and glutamate receptors, and potassium and calcium channels appear to be irrelevant or play only minor roles. Furthermore, no combination of actions on ligand- or voltage-gated channels seems sufficient. A few plausible targets (e.g., sodium channels) merit further study, but there remains the possibility that immobilization results from a nonspecific mechanism.
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