ArticleThe Journal of neuroscience : the official journal of the Society for Neuroscience2010
Anesthetic activation of central respiratory chemoreceptor neurons involves inhibition of a THIK-1-like background K(+) current.
Article in The Journal of neuroscience : the official journal of the Society for Neuroscience, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 54 papers.
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Who cites it
54 citing papers in PubMed, 83 citations in OpenAlex.
- Volatile anesthetic sedation in acute respiratory distress syndrome.Intensive care medicine · 2026Review
- K2P channels as emerging therapeutic targets for pain: insights from functional studies and transcriptomic analyses.Frontiers in pharmacology · 2026Review
- Convergent Control of NREM Sleep and Anesthesia by Prefrontal Layer 5 Extratelencephalic Neurons.Research square · 2025Article
- Review
- Structure of the human KNature structural & molecular biology · 2025Article
- Interactions between Arousal State and COThe Journal of neuroscience : the official journal of the Society for Neuroscience · 2025Article
- Volatile anaesthetics for ICU sedation: beyond hypnosis?Critical care (London, England) · 2024Article
- Volatile anesthetics for lung- and diaphragm-protective sedation.Critical care (London, England) · 2024Review
- Sodium Leak Channel in Glutamatergic Neurons of the Lateral Parabrachial Nucleus Helps to Maintain Respiratory Frequency Under Sevoflurane Anesthesia.Neuroscience bulletin · 2024Article
- Structure of the human KbioRxiv : the preprint server for biology · 2024Article
- The Modulation by Anesthetics and Analgesics of Respiratory Rhythm in the Nervous System.Current neuropharmacology · 2024Review
- General anesthetic action profile on the human prefrontal cortex cells through comprehensive single-cell RNA-seq analysis.iScience · 2023Article
- Article
- Criteria for central respiratory chemoreceptors: experimental evidence supporting current candidate cell groups.Frontiers in physiology · 2023Review
- Increased Respiratory Drive after Prolonged Isoflurane Sedation: A Retrospective Cohort Study.Journal of clinical medicine · 2022Article
- Putative Roles of Astrocytes in General Anesthesia.Current neuropharmacology · 2022Review
- Signatures of Thalamocortical Alpha Oscillations and Synchronization With Increased Anesthetic Depths Under Isoflurane.Frontiers in pharmacology · 2022Article
- Volatile anesthetics maintain tidal volume and minute ventilation to a greater degree than propofol under spontaneous respiration.BMC anesthesiology · 2021Article
- Structural Insights into the Mechanisms and Pharmacology of KJournal of molecular biology · 2021Review
- The Polysite Pharmacology of TREK KAdvances in experimental medicine and biology · 2021Article
Corrections and comments
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Authors and funding
8 authors at 3 institutions in 2 countries.
Funding
Abstract
At surgical depths of anesthesia, inhalational anesthetics cause a loss of motor response to painful stimuli (i.e., immobilization) that is characterized by profound inhibition of spinal motor circuits. Yet, although clearly depressed, the respiratory motor system continues to provide adequate ventilation under these same conditions. Here, we show that isoflurane causes robust activation of CO(2)/pH-sensitive, Phox2b-expressing neurons located in the retrotrapezoid nucleus (RTN) of the rodent brainstem, in vitro and in vivo. In brainstem slices from Phox2b-eGFP mice, the firing of pH-sensitive RTN neurons was strongly increased by isoflurane, independent of prevailing pH conditions. At least two ionic mechanisms contributed to anesthetic activation of RTN neurons: activation of an Na(+)-dependent cationic current and inhibition of a background K(+) current. Single-cell reverse transcription-PCR analysis of dissociated green fluorescent protein-labeled RTN neurons revealed expression of THIK-1 (TWIK-related halothane-inhibited K(+) channel, K(2P)13.1), a channel that shares key properties with the native RTN current (i.e., suppression by inhalational anesthetics, weak rectification, inhibition by extracellular Na(+), and pH-insensitivity). Isoflurane also increased firing rate of RTN chemosensitive neurons in urethane-anesthetized rats, again independent of CO(2) levels. In these animals, isoflurane transiently enhanced activity of the respiratory system, an effect that was most prominent at low levels of respiratory drive and mediated primarily by an increase in respiratory frequency. These data indicate that inhalational anesthetics cause activation of RTN neurons, which serve an important integrative role in respiratory control; the increased drive provided by enhanced RTN neuronal activity may contribute, in part, to maintaining respiratory motor activity under immobilizing anesthetic conditions.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.