ArticleExperimental neurobiology2015
Disinhibitory Action of Astrocytic GABA at the Perforant Path to Dentate Gyrus Granule Neuron Synapse Reverses to Inhibitory in Alzheimer's Disease Model.
Article in Experimental neurobiology, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.
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Who cites it
12 citing papers in PubMed, 25 citations in OpenAlex.
- Curing the brain: in search for new astrocyte-specific therapies.Experimental & molecular medicine · 2026Review
- Fast-spiking parvalbumin-positive interneurons in brain physiology and Alzheimer's disease.Molecular psychiatry · 2023Review
- GABA tone regulation and its cognitive functions in the brain.Nature reviews. Neuroscience · 2023Review
- GABA Release from Astrocytes in Health and Disease.International journal of molecular sciences · 2022Review
- G-Protein-Coupled Receptors in Astrocyte-Neuron Communication.Neuroscience · 2021Review
- The Paradox of Astroglial CaFrontiers in cellular neuroscience · 2020Review
- Influence of hippocampal GABAMetabolic brain disease · 2018Article
- Control of motor coordination by astrocytic tonic GABA release through modulation of excitation/inhibition balance in cerebellum.Proceedings of the National Academy of Sciences of the United States of America · 2018Article
- Reactive Astrocytes as Drug Target in Alzheimer's Disease.BioMed research international · 2018Review
- Article
- Involvement of Astrocytes in Alzheimer's Disease from a Neuroinflammatory and Oxidative Stress Perspective.Frontiers in molecular neuroscience · 2017Review
- Neuronal Expression and Cell-Type-Specific Gene-Silencing of Best1 in Thalamic Reticular Nucleus Neurons Using pSico-Red System.Experimental neurobiology · 2016Article
Corrections and comments
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Authors and funding
5 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Like neurons, astrocytes produce and release GABA to influence neuronal signaling. At the perforant path to dentate gyrus granule neuron synapse, GABA from astrocyte was found to be a strong inhibitory factor, which impairs synaptic transmission, synaptic plasticity and memory in Alzheimer's disease. Although astrocytic GABA is observed in many brain regions, its physiological role has not been clearly demonstrated yet. Here, we show that astrocytic GABA exerts disinhibitory action to dentate granule neurons by targeting GABAB receptors of GABAergic interneurons in wild-type mice. This disinhibitory effect is specific to a low intensity of electrical stimulation at perforant path fibers. Inversely in Alzheimer's disease model mice, astrocytic GABA targets GABAA receptors and exerts inhibitory action by reducing release probability of glutamatergic perforant path terminals. These results suggest that astrocytic GABA differentially modulates the signaling from cortical input to dentate gyrus under physiological and pathological conditions.
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