ArticleAnesthesiology2009
Propofol facilitates glutamatergic transmission to neurons of the ventrolateral preoptic nucleus.
Article in Anesthesiology, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 30 papers.
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Who cites it
30 citing papers in PubMed, 44 citations in OpenAlex.
- A Brainstem-Thalamic-Cortex Glutamatergic Neuron Pathway Modulates Propofol Anesthesia.Drug design, development and therapy · 2026Article
- Parafacial GABAergic neurone ablation induces behavioural resistance to volatile anaesthetic-induced hypnosis without reducing sleep.British journal of anaesthesia · 2025Article
- Neural Network Mechanisms Underlying General Anesthesia: Cortical and Subcortical Nuclei.Neuroscience bulletin · 2024Review
- Review
- Divergent Neural Activity in the VLPO During Anesthesia and Sleep.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2023Article
- Estrogen Receptor-A in Medial Preoptic Area Contributes to Sex Difference of Mice in Response to Sevoflurane Anesthesia.Neuroscience bulletin · 2022Article
- The Sleep-Promoting Ventrolateral Preoptic Nucleus: What Have We Learned over the Past 25 Years?International journal of molecular sciences · 2022Review
- A single nucleotide polymorphism-based formula to predict the risk of propofol TCI concentration being over 4 µg mLThe pharmacogenomics journal · 2022Article
- Activation of Preoptic Tachykinin 1 Neurons Promotes Wakefulness over Sleep and Volatile Anesthetic-Induced Unconsciousness.Current biology : CB · 2021Article
- The Effects of Gene Variations ofPharmacogenomics and personalized medicine · 2021Article
- Preoptic Area Modulation of Arousal in Natural and Drug Induced Unconscious States.Frontiers in neuroscience · 2021Review
- The Biology of General Anesthesia from Paramecium to Primate.Current biology : CB · 2019Review
- Towards a Comprehensive Understanding of Anesthetic Mechanisms of Action: A Decade of Discovery.Trends in pharmacological sciences · 2019Review
- Propofol decreases the excitability of cholinergic neurons in mouse basal forebrain via GABAActa pharmacologica Sinica · 2019Article
- Escape From Oblivion: Neural Mechanisms of Emergence From General Anesthesia.Anesthesia and analgesia · 2019Review
- GABAergic ventrolateral pre‑optic nucleus neurons are involved in the mediation of the anesthetic hypnosis induced by propofol.Molecular medicine reports · 2017Article
- Brainstem Influence on Thalamocortical Oscillations during Anesthesia Emergence.Frontiers in systems neuroscience · 2017Article
- The ventrolateral preoptic nucleus is required for propofol-induced inhibition of locus coeruleus neuronal activity.Neurological sciences : official journal of the Italian Neurological Society and of the Italian Society of Clinical Neurophysiology · 2015Article
- Comparison of the neuropsychological mechanisms of 2,6-diisopropylphenol and N-methyl-D-aspartate receptor antagonist against electroconvulsive therapy-induced learning and memory impairment in depressed rats.Molecular medicine reports · 2015Article
- Muscarinic M1 receptors regulate propofol modulation of GABAergic transmission in rat ventrolateral preoptic neurons.Journal of molecular neuroscience : MN · 2015Article
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
Abstract
backgroundThere 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.
methodsSpontaneous excitatory postsynaptic currents were recorded from VLPO cells-principally mechanically isolated, but also in slices from rats.
resultsIn 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.
conclusionPropofol 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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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.