ArticleInternational journal of molecular sciences2020
A Metabolic Mechanism for Anaesthetic Suppression of Cortical Synaptic Function in Mouse Brain Slices-A Pilot Investigation.
Article in International journal of molecular sciences, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
4 citing papers in PubMed, 7 citations in OpenAlex.
- Clinical Electroencephalography for Anesthesiologists and Intensivists: Part 2-Physiologic Signatures and Active Management.Anesthesiology · 2025Review
- Protective down-regulated states in the human brain: A possible lesson from COVID-19.Proceedings of the National Academy of Sciences of the United States of America · 2022Article
- Non-NMDA Mechanisms of Analgesia in Ketamine Analogs.Frontiers in pain research (Lausanne, Switzerland) · 2022Article
- Understanding the Effects of Anesthesia on Cortical Electrophysiological Recordings: A Scoping Review.International journal of molecular sciences · 2021Article
Corrections and comments
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Authors and funding
2 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Regulation of synaptically located ionotropic receptors is thought to be the main mechanism by which anaesthetics cause unconsciousness. An alternative explanation, which has received much less attention, is that of primary anaesthetic disruption of brain metabolism via suppression of mitochondrial proteins. In this pilot study in mouse cortical slices, we investigated the effect of disrupting cellular metabolism on tissue oxygen handling and cortical population seizure-like event (SLE) activity, using the mitochondrial complex I inhibitor rotenone, and compared this to the effects of the general anaesthetics sevoflurane, propofol and ketamine. Rotenone caused an increase in tissue oxygen (98 mmHg to 157 mmHg (
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