Motoneuronal TASK channels contribute to immobilizing effects of inhalational general anesthetics
Open accessAbstract
General anesthetics cause sedation, hypnosis, and immobilization via CNS mechanisms that remain incompletely understood; contributions of particular anesthetic targets in specific neural pathways remain largely unexplored. Among potential molecular targets for mediating anesthetic actions, members of the TASK subgroup [TASK-1 (K2P3.1) and TASK-3 (K2P9.1)] of background K + channels are appealing candidates since they are expressed in CNS sites relevant to anesthetic actions and activated by clinically relevant concentrations of inhaled anesthetics. Here, we used global and conditional TASK channel single and double subunit knock-out mice to demonstrate definitively that TASK channels account for motoneuronal, anesthetic-activated K + currents and to test their contributions to sedative, hypnotic, and immobilizing anesthetic actions. In motoneurons from all knock-out mice lines, TASK-like currents were reduced and cells were less sensitive to hyperpolarizing effects of halothane and isoflurane. In an immobilization assay, higher concentrations of both halothane and isoflurane were required to render TASK knock-out animals unresponsive to a tail pinch; in assays of sedation (loss of movement) and hypnosis (loss-of-righting reflex), TASK knock-out mice showed a modest decrease in sensitivity, and only for halothane. In conditional knock-out mice, with TASK channel deletion restricted to cholinergic neurons, immobilizing actions of the inhaled anesthetics and sedative effects of halothane were reduced to the same extent as in global knock-out lines. These data indicate that TASK channels in cholinergic neurons are molecular substrates for select actions of inhaled anesthetics; for immobilization, which is spinally mediated, these data implicate motoneurons as the likely neuronal substrates.
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Deletion of TASK-1 and TASK-3 in mice is linked to partial volatile anesthetic resistance; loss of TASK-3 reduces halothane sensitivity, stabilizes wakefulness, and slows transitions into sleep.
“Although deletion of TASK-1 and TASK-3 channels in mice is also associated with partial resistance to volatile anesthetics, the specific loss of TASK-3 not only reduces sensitivity to halothane, it also appears to stabilize the awake state and slows transitions into states of endogenous sleep [51, 52].”
From The Biology of General Anesthesia from Paramecium to Primate (2019) · cites this paper as [51]
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- Authors
- Lazarenko, R. M., Willcox, S. C., Shu, S., Berg, A. P., Jevtovic-Todorovic, V., Talley, E. M., Chen, X., & Bayliss, D. A.
- Affiliations
- University of Virginia (US)
- University of Virginia Health System (US)
- Venue
- The Journal of Neuroscience
- Publisher
- Society for Neuroscience
- Published
- 2010-06-02
- Volume
- 30
- Issue
- 22
- Pages
- 7691-7704
- ISSN
- 0270-6474 (ISSN-L)
- 1529-2401
- PMC
- PMC2909781
- OpenAlex
- W2073821859
- Cited by
- 79
- References
- 45
- Citations by year
- 2026: 2 · 2025: 2 · 2024: 4 · 2023: 2 · 2022: 1 · 2021: 7 · 2020: 5 · 2019: 8 · 2017: 9 · 2016: 4 · 2015: 7 · 2014: 7 · 2013: 7 · 2012: 4
- FWCI
- 8.87
- Type
- journal article
- Language
- en
- Open access
- hybrid
- doi.org
- Licence
- Locations
- Journal of Neuroscience (publishedVersion, cc-by-nc-sa)
- PubMed Central (publishedVersion)
- PubMed (publishedVersion)
- Funders
- American Heart Association
- National Institute of General Medical Sciences (GM-66181, R01GM066181)
- Topics
- Health Sciences › Medicine › Anesthesiology and Pain Medicine › Anesthesia and Sedative Agents
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Ion channel regulation and function
- Life Sciences › Neuroscience › Developmental Neuroscience › Anesthesia and Neurotoxicity Research
- Keywords
- TASK channels, TASK-1, TASK-3, potassium channels, halothane, isoflurane, immobilization, sedation, hypnosis, motor neurons, cholinergic neurons, anesthetic targets, conditional knockout mice
- MeSH terms
- Analysis of Variance, Animals, Animals, Newborn, Brain Stem, Cell Line, Transformed, Choline O-Acetyltransferase, Dose-Response Relationship, Drug, Electric Stimulation, Female, Halothane, Humans, Hydrogen-Ion Concentration, Isoflurane, Male, Membrane Potentials, Mice, Inbred C57BL, Motor Neurons, Nerve Tissue Proteins, Gene Deletion, Mice, Knockout, Patch-Clamp Techniques, Anesthetics, Inhalation, Potassium Channels, Tandem Pore Domain, Immobility Response, Tonic, Mice, Biophysical Phenomena, In Vitro Techniques
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