ArticleScientific reports2016
Astrocytic Acid-Sensing Ion Channel 1a Contributes to the Development of Chronic Epileptogenesis.
Article in Scientific reports, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 30 papers.
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Who cites it
30 citing papers in PubMed, 41 citations in OpenAlex.
- Acid-sensing ion channels in ischemic stroke: amplifying and constraining neuronal injury in a phase-specific framework.Pflugers Archiv : European journal of physiology · 2026Review
- Acid-sensing ion channels as sensors of brain metabolic state.Pflugers Archiv : European journal of physiology · 2026Review
- Epilepsy: Molecular Pathogenesis and Emerging Therapies.MedComm · 2026Review
- Carbogen Inhalation Therapy for Epileptic Seizures: Mechanisms, Evidence, and Future Directions.CNS neuroscience & therapeutics · 2025Review
- Ketogenic diet for infantile epileptic spasms.Epilepsia open · 2025Article
- Procalcitonin contributes to hippocampal neuronal damage and impairment of LTP: implications for cognitive dysfunction in LPS-induced neuroinflammation rat model.Archives of microbiology · 2025Article
- Inhalation of 5% COActa epileptologica · 2025Article
- Astrocytic Acid-Sensing Ion Channel 1a Contributes to the Development of Epileptic Cognitive Impairment.Biomolecules · 2025Article
- Selective blockade of acid-sensing ion channel 1a can provide substantial hippocampal neuroprotection.Frontiers in cell and developmental biology · 2025Article
- Differential vulnerability among cell types in the neurovascular unit: Description and mechanisms.Journal of cerebral blood flow and metabolism : official journal of the International Society of Cerebral Blood Flow and Metabolism · 2025Review
- A pH-sensitive closed-loop nanomachine to control hyperexcitability at the single neuron level.Nature communications · 2024Article
- Aminoprocalcitonin protects against hippocampal neuronal death via preserving oxidative phosphorylation in refractory status epilepticus.Cell death discovery · 2023Article
- Review
- Acetazolamide: Old drug, new evidence?Epilepsia open · 2022Review
- Acid-Sensing Ion Channels in Glial Cells.Membranes · 2022Review
- Ketogenic Diet Alleviates Hippocampal Neurodegeneration Possibly via ASIC1a and the Mitochondria-Mediated Apoptotic Pathway in a Rat Model of Temporal Lobe Epilepsy.Neuropsychiatric disease and treatment · 2022Article
- Article
- Acid-Sensing Ion Channels: Focus on Physiological and Some Pathological Roles in the Brain.Current neuropharmacology · 2021Review
- Acid-Sensing Ion Channels: Expression and Function in Resident and Infiltrating Immune Cells in the Central Nervous System.Frontiers in cellular neuroscience · 2021Review
- Lactate as an Astroglial Signal Augmenting Aerobic Glycolysis and Lipid Metabolism.Frontiers in physiology · 2021Review
Corrections and comments
- Erratum issued
Authors and funding
10 authors at 4 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Unraveling mechanisms underlying epileptogenesis after brain injury is an unmet medical challenge. Although histopathological studies have revealed that reactive astrogliosis and tissue acidosis are prominent features in epileptogenic foci, their roles in epileptogenesis remain unclear. Here, we explored whether astrocytic acid-sensing ion channel-1a (ASIC1a) contributes to the development of chronic epilepsy. High levels of ASIC1a were measured in reactive astrocytes in the hippocampi of patients with temporal lobe epilepsy (TLE) and epileptic mice. Extracellular acidosis caused a significant Ca(2+) influx in cultured astrocytes, and this influx was sensitive to inhibition by the ASIC1a-specific blocker psalmotoxin 1 (PcTX1). In addition, recombinant adeno-associated virus (rAAV) vectors carrying a GFAP promoter in conjunction with ASIC1a shRNA or cDNA were generated to suppress or restore, respectively, ASIC1a expression in astrocytes. Injection of rAAV-ASIC1a-shRNA into the dentate gyrus of the wide type TLE mouse model resulted in the inhibition of astrocytic ASIC1a expression and a reduction in spontaneous seizures. By contrast, rAAV-ASIC1a-cDNA restored astrocytic ASIC1a expression in an ASIC1a knock-out TLE mouse model and increased the frequency of spontaneous seizures. Taken together, our results reveal that astrocytic ASIC1a may be an attractive new target for the treatment of epilepsy.
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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.