ArticleFrontiers in cellular neuroscience2019
Ketamine Within Clinically Effective Range Inhibits Glutamate Transmission From Astrocytes to Neurons and Disrupts Synchronization of Astrocytic SICs.
Article in Frontiers in cellular neuroscience, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
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Who cites it
9 citing papers in PubMed, 18 citations in OpenAlex.
- NMDA receptor mediated tonic excitatory currents are elicited by EAAT inhibition on human neocortical pyramidal neurons.Frontiers in synaptic neuroscience · 2026Article
- The Behavioral and Neuroinflammatory Impact of Ketamine in a Murine Model of Depression and Liver Damage.International journal of molecular sciences · 2025Article
- Glial-Neuronal Interaction in Synapses: A Possible Mechanism of the Pathophysiology of Bipolar Disorder.Advances in experimental medicine and biology · 2023Review
- Astrocyte regulation of synaptic signaling in psychiatric disorders.Neuropsychopharmacology : official publication of the American College of Neuropsychopharmacology · 2023Review
- Putative Roles of Astrocytes in General Anesthesia.Current neuropharmacology · 2022Review
- Ketamine Alters Functional Plasticity of Astroglia: An Implication for Antidepressant Effect.Life (Basel, Switzerland) · 2021Review
- Crocins, the Bioactive Components ofMolecules (Basel, Switzerland) · 2021Article
- Ketamine Action on Astrocytes Provides New Insights into Rapid Antidepressant Mechanisms.Advances in neurobiology · 2021Review
- Neuron-Glia Crosstalk Plays a Major Role in the Neurotoxic Effects of KetamineFrontiers in cell and developmental biology · 2021Article
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Authors and funding
8 authors at 2 institutions in 1 country.
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No grant is acknowledged in the PubMed record.
Abstract
backgroundAstrocytes are now considered as crucial modulators of neuronal synaptic transmission. General anesthetics have been found to inhibit astrocytic activities, but it is not clear whether general anesthetics within the clinical concentration range affects the astrocyte-mediated synaptic regulation.
methodsThe effects of propofol, dexmedetomidine, and ketamine within clinically effective ranges on the slow inward currents (SICs) were tested by using the whole-cell recording in acute prefrontal cortex (PFC) slice preparations of rats. Astrocytes culture and HPLC were used to measure the effects of different anesthetics on the glutamate release of astrocytes.
resultsPropofol and dexmedetomidine showed no significant effect on the amplitude or frequency of SICs. Ketamine was found to inhibit the frequency of SICs in a concentration-dependent manner. The SICs synchronization rate of paired neurons was inhibited by 30 μM ketamine (from 42.5 ± 1.4% to 9.6 ± 0.8%) and was abolished by 300 μM ketamine. The astrocytic glutamate release induced by DHPG, an agonist of astrocytic type I metabotropic glutamate receptors, was not affected by ketamine, and ifenprodil, a selective antagonist of GluN1/GluN2B receptor, blocked all SICs and enhanced the inhibitory effect of 30 μM ketamine on the frequency of SICs. Ketamine at low concentration (3 μM) could inhibit the frequency of SICs, not the miniature excitatory postsynaptic currents (mEPSCs), and the inhibition rate of SICs was significantly higher than mEPSCs with 30 μM ketamine (44.5 ± 3% inhibition vs. 28.3 ± 6% inhibition).
conclusionOur data indicated that ketamine, not propofol and dexmedetomidine, within clinical concentration range inhibits glutamatergic transmission from astrocytes to neurons, which is likely mediated by the extrasynaptic GluN1/GluN2B receptor activation.
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