Tonic inhibition in dentate gyrus impairs long-term potentiation and memory in an Alzheimer’s disease model
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Amyloid plaques and tau tangles are common pathological hallmarks for Alzheimer's disease (AD); however, reducing Aβ production failed to relieve the symptoms of AD patients. Here we report a high GABA (γ-aminobutyric acid) content in reactive astrocytes in the dentate gyrus (DG) of a mouse model for AD (5xFAD) that results in increased tonic inhibition and memory deficit. We also confirm in human AD patient brains that dentate astrocytes have a high GABA content, suggesting that high astrocytic GABA level may be a novel biomarker and a potential diagnostic tool for AD. The excessive GABA in 5xFAD astrocytes is released through an astrocyte-specific GABA transporter GAT3/4, and significantly enhances tonic GABA inhibition in dentate granule cells. Importantly, reducing tonic inhibition in 5xFAD mice rescues the impairment of long-term potentiation (LTP) and memory deficit. Thus, reducing tonic GABA inhibition in the DG may lead to a novel therapy for AD.
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Reactive astrocytes surrounding Aβ deposits show enhanced synthesis and release of GABA, which increases tonic inhibition of dentate granule cells and negatively impacts memory processing.
“Another signaling aberration seen in reactive astrocytes sur rounding Aβ deposits consists in an enhanced synthesis and release of the transmitter GABA 103-105 , which increases tonic inhibition of dentate granule cells with a negative impact on memory processing.”
From Astrocyte function from information processing to cognition and cognitive impairment (2019) · cites this paper as [104]
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- Authors
- Wu, Z., Guo, Z., Gearing, M., & Chen, G.
- Affiliations
- Pennsylvania State University (US)
- Emory University (US)
- Corresponding author
- Chen, Gong
- Venue
- Nature Communications
- Published
- 2014-06-13
- Volume
- 5
- Issue
- 1
- Pages
- 4159-4159
- ISSN
- 2041-1723 (ISSN-L)
- PMC
- PMC4159602
- OpenAlex
- W1985097707
- Cited by
- 306
- References
- 64
- Citations by year
- 2026: 16 · 2025: 23 · 2024: 20 · 2023: 26 · 2022: 26 · 2021: 38 · 2020: 42 · 2019: 25 · 2018: 27 · 2017: 31 · 2016: 15 · 2015: 12 · 2014: 5
- FWCI
- 14.00
- Type
- journal article
- Language
- en
- Update notices
- correction (2014-09-12)
- Open access
- bronze
- doi.org
- Licence
- Locations
- Nature Communications (publishedVersion)
- PubMed (publishedVersion)
- Europe PMC (PubMed Central) (acceptedVersion)
- PubMed Central (acceptedVersion)
- RePEc: Research Papers in Economics (submittedVersion)
- Funders
- National Institutes of Health (AG045656, AG025688, NS055077)
- National Institute on Aging (AG045656, R01AG045656, P50AG025688)
- National Institute of Mental Health (R01MH083911, MH083911)
- National Institute of Neurological Disorders and Stroke (P30NS055077)
- Topics
- Health Sciences › Medicine › Physiology › Alzheimer's disease research and treatments
- Life Sciences › Neuroscience › Cellular and Molecular Neuroscience › Neuroscience and Neuropharmacology Research
- Life Sciences › Neuroscience › Neurology › Neuroinflammation and Neurodegeneration Mechanisms
- Keywords
- Alzheimer's disease, tonic inhibition, dentate gyrus, astrocytes, GABA, 5xFAD mice, long-term potentiation, memory impairment, GABA transporters, GAT-3, dentate gyrus granule cells, biomarkers, GABAergic neurotransmission
- MeSH terms
- Alzheimer Disease, Animals, Astrocytes, Disease Models, Animal, Female, gamma-Aminobutyric Acid, Humans, Male, Memory, Mice, Inbred C57BL, Mice, Transgenic, Receptors, GABA-A, Long-Term Potentiation, Dentate Gyrus, Mice
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