Astrocytic adenosine receptor A2A and Gs-coupled signaling regulate memory
Open accessAbstract
Astrocytes express a variety of G protein-coupled receptors and might influence cognitive functions, such as learning and memory. However, the roles of astrocytic Gs-coupled receptors in cognitive function are not known. We found that humans with Alzheimer's disease (AD) had increased levels of the Gs-coupled adenosine receptor A2A in astrocytes. Conditional genetic removal of these receptors enhanced long-term memory in young and aging mice and increased the levels of Arc (also known as Arg3.1), an immediate-early gene that is required for long-term memory. Chemogenetic activation of astrocytic Gs-coupled signaling reduced long-term memory in mice without affecting learning. Like humans with AD, aging mice expressing human amyloid precursor protein (hAPP) showed increased levels of astrocytic A2A receptors. Conditional genetic removal of these receptors enhanced memory in aging hAPP mice. Together, these findings establish a regulatory role for astrocytic Gs-coupled receptors in memory and suggest that AD-linked increases in astrocytic A2A receptor levels contribute to memory loss.
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Mice in which astrocyte Gs signaling is selectively stimulated show the opposite memory effect to A2A receptor loss or antagonism.
“whereas mice in which astrocyte Gs signaling is selectively stimulated (Table 1) show the opposite 99”
From Astrocyte function from information processing to cognition and cognitive impairment (2019) · cites this paper as [99]
A2A adenosine receptors are up-regulated in astrocytes in AD and signal via Gs-cAMP.
“A2A adenosine receptors 99 , which instead signal via Gs-cAMP.”
From Astrocyte function from information processing to cognition and cognitive impairment (2019) · cites this paper as [99]
Excessive activation of A2A receptors in AD may accentuate the forgetting pathway and result in reduced memory performance.
“However, when excessively activated in AD 99 , A2A receptors may accentuate the 'forgetting pathway' resulting in reduced memory performance.”
From Astrocyte function from information processing to cognition and cognitive impairment (2019) · cites this paper as [99]
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- Authors
- Orr, A. G., Hsiao, E. C., Wang, M. M., Ho, K., Kim, D. H., Wang, X., Guo, W., Kang, J., Yu, G.-Q., Adame, A., Devidze, N., Dubal, D. B., Masliah, E., Conklin, B. R., & Mucke, L.
- Affiliations
- Gladstone Institutes (US)
- University of California San Diego (US)
- University of California, San Francisco (US)
- Corresponding author
- Orr, Anna G
- Mucke, Lennart
- ORCID
- Venue
- Nature Neuroscience
- Published
- 2015-01-26
- Volume
- 18
- Issue
- 3
- Pages
- 423-434
- ISSN
- 1097-6256 (ISSN-L)
- 1546-1726
- PMC
- PMC4340760
- OpenAlex
- W2050513958
- Cited by
- 289
- References
- 87
- Citations by year
- 2026: 20 · 2025: 22 · 2024: 19 · 2023: 26 · 2022: 23 · 2021: 34 · 2020: 21 · 2019: 23 · 2018: 33 · 2017: 30 · 2016: 28 · 2015: 9
- FWCI
- 24.54
- Type
- journal article
- Language
- en
- Open access
- green
- www.ncbi.nlm.nih.gov
- Licence
- www.springer.com/tdm (tdm)
- Locations
- Nature Neuroscience (publishedVersion)
- PubMed (publishedVersion)
- PubMed Central (acceptedVersion)
- eScholarship (California Digital Library) (submittedVersion)
- Funders
- National Institute on Aging (K08AG034531, P50AG005131, AG022074, P01AG022074, AG039220, AG034531, F32AG039220)
- National Heart, Lung, and Blood Institute (R01HL060664, U01HL100406, HL60664, HL100406)
- National Institute of Mental Health (R01MH062962)
- National Institute of Neurological Disorders and Stroke (NS065780, P30NS065780)
- National Institute of Arthritis and Musculoskeletal and Skin Diseases (K08AR056299, AR056299)
- National Center for Research Resources (RR18938)
- 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 › Cognitive Neuroscience › Memory and Neural Mechanisms
- Keywords
- astrocytes, adenosine A2A receptor, long-term memory, Alzheimer's disease, aging, Arc/Arg3.1, immediate early genes, amyloid precursor protein, chemogenetic activation, conditional gene deletion, memory loss
- MeSH terms
- Alzheimer Disease, Animals, Animals, Newborn, Astrocytes, Cytoskeletal Proteins, Exploratory Behavior, Gene Expression Regulation, Glial Fibrillary Acidic Protein, Humans, Indoles, Mice, Inbred C57BL, Mice, Transgenic, Nerve Tissue Proteins, Serotonin Antagonists, Sulfonamides, Signal Transduction, Maze Learning, Recognition, Psychology, Receptor, Adenosine A2A, Receptors, Serotonin, 5-HT4, Mice, Memory, Long-Term
About these checks
Registry, retraction, Cites and statistics results are computed, not judged, with one exception: a printed reference that no index lists is read once by a model before it counts as a citation error. Claims are extracted by a model and kept only when their quote appears verbatim in the text; each cited source is then checked, with a model’s help, for whether it says what the claim relies on. Those verdicts can be wrong — read the claim’s quote and the cited source before relying on one.
Statistics and arithmetic are recomputed, not judged.
Confidence bands are shown only for fields calibrated on our annotated test set. None is calibrated yet, so no band is shown.
What counts as a claim ›How we measure confidence ›How we check this ›
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