ArticleThe Journal of physiology2014
Glial GABA, synthesized by monoamine oxidase B, mediates tonic inhibition.
Article in The Journal of physiology, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 98 papers, 1 of them a synthesis that pooled it.
What it found
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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.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
98 citing papers in PubMed, 1 synthesis or guideline pooled it, 173 citations in OpenAlex.
- Neurotransmission-related gene expression in the frontal pole is altered in subjects with bipolar disorder and schizophrenia.Translational psychiatry · 2023Pooled it
- Article
- Glial-neuronal crosstalk via GABA signaling: mechanistic insights into neuropsychiatric and neurological pathophysiology.Molecular psychiatry · 2026Review
- Curing the brain: in search for new astrocyte-specific therapies.Experimental & molecular medicine · 2026Review
- Article
- ALDH2-mediated GABA biosynthesis regulates hippocampal LTP and learning adaptability.Nature chemical biology · 2026Article
- Re-Evaluation of the Ultrastructural Localization of Tonic GABA-A Receptors.Pharmaceuticals (Basel, Switzerland) · 2025Review
- Oral KDS2010, a Monoamine Oxidase-B (MAO-B) Inhibitor, Slows the Deterioration of Motor Coordination in Genetic SCA1 Models by Inhibiting Astrocytic MAO-B-Mediated Inflammation.Journal of neurochemistry · 2025Article
- SLC45A4 encodes a peroxisomal putrescine transporter that promotes GABA de novo synthesis.Nature communications · 2025Article
- Dynamic and Homeostatic Neuron-Astrocyte Interactions at GABAergic Synapses.Neurochemical research · 2025Review
- Hemoglobin as a pseudoperoxidase and drug target for oxidative stress-related diseases.Signal transduction and targeted therapy · 2025Article
- Astrocytic gamma-aminobutyric acid dysregulation as a therapeutic target for posttraumatic stress disorder.Signal transduction and targeted therapy · 2025Article
- Astrocytic BEST1 can serve as a target for functional recovery after ischemic stroke.Molecular therapy : the journal of the American Society of Gene Therapy · 2025Article
- The Role of Astrocytes in Synaptic Dysfunction and Memory Deficits in Alzheimer's Disease.Biomolecules · 2025Review
- Neuroimmune regulation of the prefrontal cortex tetrapartite synapse.Neuropharmacology · 2025Review
- Astrocyte Dysfunctions in Obsessive Compulsive Disorder: Rethinking Neurobiology and Therapeutic Targets.Journal of neurochemistry · 2025Review
- Article
- Suppressing astrocytic GABA transaminase enhances tonic inhibition and weakens hippocampal spatial memory.Experimental & molecular medicine · 2025Article
- Regulation of GABAergic neurotransmission by purinergic receptors in brain physiology and disease.Purinergic signalling · 2025Review
- SIRT2 and ALDH1A1 as critical enzymes for astrocytic GABA production in Alzheimer's disease.Molecular neurodegeneration · 2025Article
38 more citing papers are in PubMed but not listed here.
Corrections and comments
- Erratum issuedCorrigendum.2021
Authors and funding
15 authors at 5 institutions in 1 country.
Funding
Abstract
GABA is the major inhibitory transmitter in the brain and is released not only from a subset of neurons but also from glia. Although neuronal GABA is well known to be synthesized by glutamic acid decarboxylase (GAD), the source of glial GABA is unknown. After estimating the concentration of GABA in Bergmann glia to be around 5-10 mM by immunogold electron microscopy, we demonstrate that GABA production in glia requires MAOB, a key enzyme in the putrescine degradation pathway. In cultured cerebellar glia, both Ca(2+)-induced and tonic GABA release are significantly reduced by both gene silencing of MAOB and the MAOB inhibitor selegiline. In the cerebellum and striatum of adult mice, general gene silencing, knock out of MAOB or selegiline treatment resulted in elimination of tonic GABA currents recorded from granule neurons and medium spiny neurons. Glial-specific rescue of MAOB resulted in complete rescue of tonic GABA currents. Our results identify MAOB as a key synthesizing enzyme of glial GABA, which is released via bestrophin 1 (Best1) channel to mediate tonic inhibition in the brain.
Indexed as
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What OpenQuestion holds
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.