Neuron–astrocyte signaling is preserved in the aging brain
Open accessAbstract
Astrocytes play crucial roles in brain homeostasis and are emerging as regulatory elements of neuronal and synaptic physiology by responding to neurotransmitters with Ca 2+ elevations and releasing gliotransmitters that activate neuronal receptors. Aging involves neuronal and astrocytic alterations, being considered risk factor for neurodegenerative diseases. Most evidence of the astrocyte–neuron signaling is derived from studies with young animals; however, the features of astrocyte–neuron signaling in adult and aging brain remain largely unknown. We have investigated the existence and properties of astrocyte–neuron signaling in physiologically and pathologically aging mouse hippocampal and cortical slices at different lifetime points (0.5 to 20 month‐old animals). We found that astrocytes preserved their ability to express spontaneous and neurotransmitter‐dependent intracellular Ca 2+ signals from juvenile to aging brains. Likewise, resting levels of gliotransmission, assessed by neuronal NMDAR activation by glutamate released from astrocytes, were largely preserved with similar properties in all tested age groups, but DHPG‐induced gliotransmission was reduced in aged mice. In contrast, gliotransmission was enhanced in the APP/PS1 mouse model of Alzheimer's disease, indicating a dysregulation of astrocyte–neuron signaling in pathological conditions. Disruption of the astrocytic IP 3 R2 mediated‐signaling, which is required for neurotransmitter‐induced astrocyte Ca 2+ signals and gliotransmission, boosted the progression of amyloid plaque deposits and synaptic plasticity impairments in APP/PS1 mice at early stages of the disease. Therefore, astrocyte–neuron interaction is a fundamental signaling, largely conserved in the adult and aging brain of healthy animals, but it is altered in Alzheimer's disease, suggesting that dysfunctions of astrocyte Ca 2+ physiology may contribute to this neurodegenerative disease. GLIA 2017 GLIA 2017;65:569–580
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Astrocytes in apposition to Aβ deposits are hyperactive and display higher resting Ca2+ levels, more frequent and larger Ca2+ elevations, long-range coordinated Ca2+ waves never seen in control mice, and increased gliotransmission.
“Interestingly, astrocytes in apposition to Aβ deposits are also 'hyperactive' and display higher resting Ca 2+ level, more frequent and larger Ca 2+ elevations, long-range coordinated Ca 2+ waves that are never seen in control mice 95, 98, 111 , as well as increased gliotranmission 112 .”
From Astrocyte function from information processing to cognition and cognitive impairment (2019) · cites this paper as [112]
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Self-citation
- Authors
- Gómez‐Gonzalo, M., Martin‐Fernandez, M., Martínez‐Murillo, R., Mederos, S., Hernández‐Vivanco, A., Jamison, S., Fernandez, A. P., Serrano, J., Calero, P., Futch, H. S., Corpas, R., Sanfeliu, C., Perea, G., & Araque, A.
- Affiliations
- Consejo Superior de Investigaciones Científicas (ES)
- Department of Neuroscience University of Minnesota Minneapolis 55455
- University of Minnesota (US)
- Instituto Cajal, CSIC Madrid 28002 Spain
- University of Florida (US)
- Corresponding author
- Perea, Gertrudis
- Araque, Alfonso
- ORCID
- Venue
- Glia
- Publisher
- Wiley
- Published
- 2017-01-28
- Volume
- 65
- Issue
- 4
- Pages
- 569-580
- ISSN
- 0894-1491 (ISSN-L)
- 1098-1136
- PMC
- PMC5314210
- OpenAlex
- W2580929144
- Cited by
- 114
- References
- 62
- Citations by year
- 2026: 5 · 2025: 15 · 2024: 6 · 2023: 21 · 2022: 11 · 2021: 18 · 2020: 18 · 2019: 8 · 2018: 7 · 2017: 5
- FWCI
- 5.09
- Type
- journal article
- Language
- en
- Open access
- green
- www.ncbi.nlm.nih.gov
- Locations
- Glia (publishedVersion)
- PubMed (publishedVersion)
- PubMed Central (acceptedVersion)
- DIGITAL.CSIC (Spanish National Research Council (CSIC)) (submittedVersion)
- Funders
- Research Grant (R01NS097312-01)
- NIH-NINDS (R01NS097312-01)
- Topics
- Life Sciences › Neuroscience › Cellular and Molecular Neuroscience › Neuroscience and Neuropharmacology Research
- Life Sciences › Neuroscience › Neurology › Neuroinflammation and Neurodegeneration Mechanisms
- Health Sciences › Medicine › Physiology › Alzheimer's disease research and treatments
- Keywords
- astrocyte-neuron communication, brain aging, gliotransmission, astrocyte calcium signaling, IP3R2, APP/PS1 mice, Alzheimer's disease, amyloid plaques, synaptic plasticity, NMDA receptor activation, glutamate release, hippocampus, cerebral cortex, DHPG
- MeSH terms
- Acetylcholine, Adenosine Triphosphate, Aging, Animals, Astrocytes, Brain, Calcium, Cell Communication, Membrane Potentials, Methoxyhydroxyphenylglycol, Mice, Inbred C57BL, Mice, Transgenic, Neurons, Synapses, Signal Transduction, Amyloid beta-Protein Precursor, Excitatory Amino Acid Agents, Mice, Presenilin-1, Synaptic Potentials
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