ArticleProceedings of the National Academy of Sciences of the United States of America2014
GABAρ subunits confer a bicuculline-insensitive component to GFAP+ cells of cerebellum.
Article in Proceedings of the National Academy of Sciences of the United States of America, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.
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11 citing papers in PubMed, 20 citations in OpenAlex.
- GABA Receptor Activation in Müller Glia as a Molecular Switch for Controlling VEGF-A in the Retina.ASN neuro · 2026Article
- GABAFrontiers in immunology · 2026Article
- Cerebellar and Striatal Implications in Autism Spectrum Disorders: From Clinical Observations to Animal Models.International journal of molecular sciences · 2022Review
- Organization of the ventricular zone of the cerebellum.Frontiers in cellular neuroscience · 2022Review
- Article
- Targeting GABABrain sciences · 2021Article
- Article
- Diverse Actions of Astrocytes in GABAergic Signaling.International journal of molecular sciences · 2019Review
- Antagonistic effect of dopamine structural analogues on human GABAρ1 receptor.Scientific reports · 2017Article
- GABA-ρ receptors: distinctive functions and molecular pharmacology.British journal of pharmacology · 2017Review
- A simple solution for antibody signal enhancement in immunofluorescence and triple immunogold assays.Histochemistry and cell biology · 2016Article
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Authors and funding
5 authors at 1 institution in 1 country.
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Abstract
GABA-A receptors mediating synaptic or extrasynaptic transmission are molecularly and functionally distinct, and glial cells are known to express a plethora of GABA-A subunits. Here we demonstrate that GFAP(+) cells of the granular layer of cerebellum express GABAρ subunits during early postnatal development, thereby conferring peculiar pharmacologic characteristics to GABA responses. Electron microscopy revealed the presence of GABAρ in the plasma membrane of GFAP(+) cells. In contrast, expression in the adult was restricted to Purkinje neurons and a subset of ependymal cells. Electrophysiological studies in vitro revealed that astrocytes express functional receptors with an EC50 of 52.2 ± 11.8 μM for GABA. The evoked currents were inhibited by bicuculline (100 μM) and TPMPA (IC50, 5.9 ± 0.6 μM), indicating the presence of a GABAρ component. Coimmunoprecipitation demonstrated protein-protein interactions between GABAρ1 and GABAα1, and double immunofluorescence showed that these subunits colocalize in the plasma membrane. Three populations of GABA-A receptors in astrocytes were identified: classic GABA-A, bicuculline-insensitive GABAρ, and GABA-A-GABAρ hybrids. Clusters of GABA-A receptors were distributed in the perinuclear space and along the processes of GFAP(+) cells. Time-lapse microscopy showed GABAρ2-GFP accumulation in clusters located in the soma and along the processes. The clusters were relatively immobile, with mean displacement of 9.4 ± 0.9 μm and a net distance traveled of 1-2 μm, owing mainly to directional movement or simple diffusion. Modulation of GABAρ dynamics may be a novel mechanism of extrasynaptic transmission regulating GABAergic control of GFAP(+) cells during early postnatal development.
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