ArticleMolecular brain2013
Channel-mediated astrocytic glutamate release via Bestrophin-1 targets synaptic NMDARs.
Article in Molecular brain, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 37 papers.
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Who cites it
37 citing papers in PubMed, 57 citations in OpenAlex.
- Design and Biological Evaluation of hBest1-Containing Bilayer Nanostructures.Molecules (Basel, Switzerland) · 2025Article
- Cryo-EM structures of mouse bestrophin 1 channel in closed and partially open conformations.Molecules and cells · 2025Article
- Excitotoxic Storms of Ischemic Stroke: A Non-neuronal Perspective.Molecular neurobiology · 2024Review
- GAD65 tunes the functions of Best1 as a GABA receptor and a neurotransmitter conducting channel.Nature communications · 2024Article
- Astrocytic PAR1 and mGluR2/3 control synaptic glutamate time course at hippocampal CA1 synapses.Glia · 2024Article
- Generation of Astrocyte-specific BEST1 Conditional Knockout Mouse with Reduced Tonic GABA Inhibition in the Brain.Experimental neurobiology · 2024Article
- Gene Expression at the Tripartite Synapse: Bridging the Gap Between Neurons and Astrocytes.Advances in neurobiology · 2024Review
- Astrocytic modulation of neuronal signalling.Frontiers in network physiology · 2023Review
- Article
- Glutamate Permeability of Chicken Best1.Experimental neurobiology · 2022Article
- Improved gliotransmission by increasing intracellular CaJournal of nanobiotechnology · 2022Article
- Astrocyte Gliotransmission in the Regulation of Systemic Metabolism.Metabolites · 2021Review
- GABA, but Not Bestrophin-1, Is Localized in Astroglial Processes in the Mouse Hippocampus and the Cerebellum.Frontiers in molecular neuroscience · 2020Article
- Role of the protease-activated receptor 1 in regulating the function of glial cells within central and peripheral nervous system.Journal of neural transmission (Vienna, Austria : 1996) · 2019Review
- Review
- Traumatic Stress Produces Delayed Alterations of Synaptic Plasticity in Basolateral Amygdala.Frontiers in psychology · 2019Article
- Bestrophin-3 Expression in a Subpopulation of Astrocytes in the Neonatal Brain After Hypoxic-Ischemic Injury.Frontiers in physiology · 2019Article
- Involvement of extrasynaptic glutamate in physiological and pathophysiological changes of neuronal excitability.Cellular and molecular life sciences : CMLS · 2018Review
- Activation of Astrocytic μ-opioid Receptor Elicits Fast Glutamate Release Through TREK-1-Containing K2P Channel in Hippocampal Astrocytes.Frontiers in cellular neuroscience · 2018Article
- Physiology of Astroglia.Physiological reviews · 2018Review
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Authors and funding
6 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundAstrocytes regulate neuronal excitability and synaptic activity by releasing gliotransmitters such as glutamate. Our recent study demonstrated that astrocytes release glutamate upon GPCR activation via Ca2+ activated anion channel, Bestrophin-1 (Best1). The target of Best1-mediated astrocytic glutamate has been shown to be the neuronal NMDA receptors (NMDAR). However, whether it targets synaptically or extra-synaptically localized NMDAR is not known.
findingsWe recorded spontaneous miniature excitatory postsynaptic currents (mEPSCs) from CA1 pyramidal cells to test whether Best1-mediated astrocytic glutamate targets synaptic NMDAR. An agonist of protease activated receptor 1 (PAR1) was used to induce astrocytic Ca(2+) increase and glutamate release. Firstly, we found that activation of PAR1 and subsequent release of glutamate from astrocyte does not alone increase the frequency of mEPSCs. Secondly, we found that mEPSC rise time is variable depending on the different electrotonic distances from the somatic recording site to the synaptic region where each mEPSC occurs. Two subgroups of mEPSC from CA1 pyramidal neuron by rise time were selected and analyzed. One group is fast rising mEPSCs with a rise time of 1 ~ 5 ms, representing synaptic activities arising from proximal dendrites. The other group is slowly rising mEPSCs with a rise time of 5 ~ 10 ms, representing synaptic events arising from glutamate release at synapses located in the distal dendrites. We used cell-type specific Best1 gene silencing system by Cre-loxP cleavage to dissociate the effect of neuronal and astrocytic Best1. Astrocytic Best1-mediated glutamate release by PAR1 activation did not affect decay kinetics, frequency, and amplitude of fast rising mEPSC. In contrast, PAR1 activation resulted in an NMDA receptor component to be present on slowly rising mEPSC, but did not alter frequency or amplitude.
conclusionsOur results indicate that astrocytic glutamate via Best1 channel targets and activates synaptic NMDARs.
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