ArticleMolecular neurodegeneration2017
TRPA1 channels promote astrocytic Ca
Article in Molecular neurodegeneration, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 60 papers.
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Who cites it
60 citing papers in PubMed, 95 citations in OpenAlex.
- Astrocytes Coordinate Neurovascular Coupling During Prolonged Sensory Demand via AQP4/TRPA1/BEST1/D-Serine Signaling.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- Network-Level Characterization of Spontaneous Calcium Activity in an In-Vitro Alzheimer's Disease Model.bioRxiv : the preprint server for biology · 2026Article
- Engineering RVG-modified exosomes for targeting TGF-β1 signaling in stroke recovery.Journal of translational medicine · 2026Article
- Astrocyte CaBiomolecules · 2026Review
- The rise of astrocytes: are they guardians or troublemakers of the brain disorder?Experimental & molecular medicine · 2026Review
- Article
- Electroacupuncture reduces calcium influx and inhibits endoplasmic reticulum stress by inhibiting the PKCδ-TRPA1 pathway to promote motor function recovery after spinal cord injury.Burns & trauma · 2026Article
- Astrocyte Store-Released Calcium Modulates Visual Cortex Synapse Development and Circuit Function.Research square · 2025Article
- Astrocytes as Therapeutic Targets in Neurodegenerative Disorders.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2025Review
- Current Understanding of Protein Aggregation in Neurodegenerative Diseases.International journal of molecular sciences · 2025Review
- Clusterin Regulates the Mechanisms of Neuroinflammation and Neuronal Circuit Impairment in Alzheimer's Disease.International journal of molecular sciences · 2025Review
- Amyloid-β-induced alteration of fast and localized calcium elevations in cultured astrocytes.Scientific reports · 2025Article
- Insights into the Involvement of TRPA1 Channels in the Neuro-Inflammatory Machinery of Trigeminal Neuralgia.Molecules (Basel, Switzerland) · 2025Article
- Cell Adhesion Molecule Protocadherin-γC5 Ameliorates Aβ Plaque Pathogenesis by Modulating Astrocyte Function in Alzheimer's Disease.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2025Article
- Astrocyte regulation of behavioral outputs: the versatile roles of calcium.Frontiers in cellular neuroscience · 2025Review
- Emerging roles of astrocytes in hippocampal circuitry and behavior.Frontiers in cellular neuroscience · 2025Review
- Functional Evaluation of Astrocytic Responses to Stress.Methods in molecular biology (Clifton, N.J.) · 2025Article
- Clearing Amyloid-Beta by Astrocytes: The Role of Rho GTPases Signaling Pathways as Potential Therapeutic Targets.Brain sciences · 2024Review
- Revisiting astrocytic calcium signaling in the brain.Fundamental research · 2024Review
- Astrocytes: The Stars in Neurodegeneration?Biomolecules · 2024Review
Corrections and comments
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Authors and funding
6 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundExcessive synaptic loss is thought to be one of the earliest events in Alzheimer's disease (AD). However, the key mechanisms that maintain plasticity of synapses during adulthood or initiate synapse dysfunction in AD remain unknown. Recent studies suggest that astrocytes contribute to functional changes observed during synaptic plasticity and play a major role in synaptic dysfunction but astrocytes behavior and involvement in early phases of AD remained largely undefined.
methodsWe measure astrocytic calcium activity in mouse CA1 hippocampus stratum radiatum in both the global astrocytic population and at a single cell level, focusing in the highly compartmentalized astrocytic arbor. Concurrently, we measure excitatory post-synaptic currents in nearby pyramidal neurons.
resultsWe find that application of soluble Aβ oligomers (Aβo) induced fast and widespread calcium hyperactivity in the astrocytic population and in the microdomains of the astrocyte arbor. We show that astrocyte hyperactivity is independent of neuronal activity and is repaired by transient receptor potential A1 (TRPA1) channels blockade. In return, this TRPA1 channels-dependent hyperactivity influences neighboring CA1 neurons triggering an increase in glutamatergic spontaneous activity. Interestingly, in an AD mouse model (APP/PS1-21 mouse), astrocyte calcium hyperactivity equally takes place at the beginning of Aβ production, depends on TRPA1 channels and is linked to CA1 neurons hyperactivity.
conclusionsOur experiments demonstrate that astrocytes contribute to early Aβo toxicity exhibiting a global and local Ca
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.