Propofol facilitates glutamatergic transmission to neurons of the ventrolateral preoptic nucleus
Open accessAbstract
Background: There is much evidence that the sedative component of anesthesia is mediated by gamma-aminobutyric acid type A (GABA(A)) receptors on hypothalamic neurons responsible for arousal, notably in the tuberomammillary nucleus. These GABA(A) receptors are targeted by gamma-aminobutyric acid-mediated (GABAergic) neurons in the ventrolateral preoptic area (VLPO): When these neurons become active, they inhibit the arousal-producing nuclei and induce sleep. According to recent studies, propofol induces sedation by enhancing VLPO-induced synaptic inhibition, making the target cells more responsive to GABA(A). The authors explored the possibility that propofol also promotes sedation less directly by facilitating excitatory inputs to the VLPO GABAergic neurons. Methods: Spontaneous excitatory postsynaptic currents were recorded from VLPO cells-principally mechanically isolated, but also in slices from rats. Results: In isolated VLPO GABAergic neurons, propofol increased the frequency of glutamatergic spontaneous excitatory postsynaptic currents without affecting their mean amplitude. The action of propofol was mimicked by muscimol and prevented by gabazine, respectively a specific agonist and antagonist at GABA(A) receptors. It was also suppressed by bumetanide, a blocker of Na-K-Cl cotransporter-mediated inward Cl transport. In slices, propofol also increased the frequency of spontaneous excitatory postsynaptic currents and, at low doses, accelerated firing of VLPO cells. Conclusion: Propofol induces sedation, at least in part, by increasing firing of GABAergic neurons in the VLPO, indirectly by activation of GABA(A) receptors on glutamatergic afferents: Because these axons/terminals have a relatively high internal Cl concentration, they are depolarized by GABAergic agents such as propofol, which thus enhance glutamate release.
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Except for ketamine, systemic hypnotic doses of every general anesthetic examined recruit sleep-promoting VLPO neurons.
“with the exception of ketamine, systemic delivery of hypnotic doses of every general anesthetic examined recruits sleep-promoting neurons in the VLPO [98–102]”
From The Biology of General Anesthesia from Paramecium to Primate (2019) · cites this paper as [102]
Sleep-promoting VLPO neurons are depolarized by isoflurane and other anesthetics.
“sleep-promoting VLPO neurons were depolarized by isoflurane and other anesthetics [99, 102].”
From The Biology of General Anesthesia from Paramecium to Primate (2019) · cites this paper as [102]
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- Authors
- Li, K. Y., Guan, Y.-Z., Krnjević, K., & Ye, J. H.
- Affiliations
- Postdoctoral Fellow.
- Professor, Department of Physiology, McGill University, Montreal, Quebec, Canada.
- Rutgers New Jersey Medical School (US)
- Venue
- Anesthesiology
- Published
- 2009-12-01
- Volume
- 111
- Issue
- 6
- Pages
- 1271-1278
- ISSN
- 0003-3022 (ISSN-L)
- PMC
- PMC2798160
- OpenAlex
- W2093126183
- Cited by
- 45
- References
- 53
- Citations by year
- 2026: 1 · 2025: 3 · 2024: 1 · 2023: 2 · 2022: 4 · 2021: 3 · 2020: 1 · 2019: 3 · 2018: 3 · 2017: 2 · 2016: 2 · 2015: 4 · 2014: 5 · 2013: 4 · 2012: 3
- FWCI
- 2.68
- Type
- journal article
- Language
- en
- Open access
- bronze
- doi.org
- Locations
- Anesthesiology (publishedVersion)
- PubMed (publishedVersion)
- Europe PMC (PubMed Central) (acceptedVersion)
- PubMed Central (acceptedVersion)
- Funders
- National Institutes of Health
- National Institute on Alcohol Abuse and Alcoholism (AA016964, R21AA015925, R01AA016964)
- Topics
- Health Sciences › Medicine › Anesthesiology and Pain Medicine › Anesthesia and Sedative Agents
- Life Sciences › Neuroscience › Cellular and Molecular Neuroscience › Neuroscience and Neuropharmacology Research
- Life Sciences › Neuroscience › Developmental Neuroscience › Anesthesia and Neurotoxicity Research
- Keywords
- propofol, ventrolateral preoptic nucleus, glutamatergic neurotransmission, GABAergic neurons, GABAA receptor, sedation, glutamatergic afferents, excitatory postsynaptic currents, muscimol, gabazine, bumetanide, Na+-K+-2Cl- cotransporter, chloride transport, sleep induction, arousal
- MeSH terms
- Anesthetics, Local, Animals, Cadmium, Electrophysiology, Glutamates, Synaptic Transmission, Neurons, Preoptic Area, Tetrodotoxin, Propofol, Rats, Sprague-Dawley, Patch-Clamp Techniques, Anesthetics, Intravenous, GABA Agonists, GABA Antagonists, Excitatory Postsynaptic Potentials, Sodium-Potassium-Chloride Symporters, Rats, In Vitro Techniques
About these checks
Registry, retraction, Cites and statistics results are computed, not judged, with one exception: a printed reference that no index lists is read once by a model before it counts as a citation error. Claims are extracted by a model and kept only when their quote appears verbatim in the text; each cited source is then checked, with a model’s help, for whether it says what the claim relies on. Those verdicts can be wrong — read the claim’s quote and the cited source before relying on one.
Statistics and arithmetic are recomputed, not judged.
Confidence bands are shown only for fields calibrated on our annotated test set. None is calibrated yet, so no band is shown.
What counts as a claim ›How we measure confidence ›How we check this ›
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