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Is a new paradigm needed to explain how inhaled anesthetics produce immobility?

TitleIs a new paradigm needed to explain how inhaled anesthetics produce immobility?
Publication TypeJournal Article
Year of Publication2008
AuthorsEger EI, Raines DE, Shafer SL, Hemmings HC, Sonner JM
JournalAnesth Analg
Date Published2008 Sep
KeywordsAnalgesia, Anesthetics, Inhalation, Animals, Humans, Immobilization, Ligands, Mice, Models, Biological, Models, Genetic, Models, Theoretical, Receptors, GABA-A, Receptors, Glutamate, Receptors, Serotonin, 5-HT3, Sodium Channels, Static Electricity

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, gamma-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.

Alternate JournalAnesth. Analg.
PubMed ID18713892
PubMed Central IDPMC2653203
Grant List1P01GM47818 / GM / NIGMS NIH HHS / United States
P01 GM047818-14 / GM / NIGMS NIH HHS / United States
R01 GM058055 / GM / NIGMS NIH HHS / United States