ArticleThe Journal of neuroscience : the official journal of the Society for Neuroscience2019
Inorganic Polyphosphate Regulates AMPA and NMDA Receptors and Protects Against Glutamate Excitotoxicity via Activation of P2Y Receptors.
Article in The Journal of neuroscience : the official journal of the Society for Neuroscience, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 papers.
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Who cites it
28 citing papers in PubMed, 45 citations in OpenAlex.
- Inorganic polyphosphate chelates CaBiochemistry and biophysics reports · 2026Article
- Review
- Inorganic Polyphosphate and Human Diseases.Progress in molecular and subcellular biology · 2026Review
- Molecular mechanisms of excitotoxicity and their relevance to the pathogenesis of neurodegenerative diseases-an update.Acta pharmacologica Sinica · 2025Review
- Mitochondrial calcium overload is the trigger for carbon monoxide neurotoxicity.Cell death & disease · 2025Article
- Inorganic Polyphosphate: An Emerging Regulator of Neuronal Bioenergetics and Its Implications in Neuroprotection.Biomolecules · 2025Review
- Mitochondrial Calcium Uniporter (MCU)-Mediated Calcium Overload in Psychoactive Drug Neurotoxicity: From Pathogenesis to Therapeutic Targets.International journal of molecular sciences · 2025Review
- Short-chain polyphosphates induce tau fibrillation and neurotoxicity in human iPSC-derived retinal neurons.Cell death & disease · 2025Article
- The Protein Scaffolding Functions of Polyphosphate.Journal of molecular biology · 2024Review
- PRUNE1 and NME/NDPK family proteins influence energy metabolism and signaling in cancer metastases.Cancer metastasis reviews · 2024Review
- Inflammatory Factor IL1α Induces Aberrant Astrocyte Proliferation in Spinal Cord Injury Through the Grin2c/CaNeuroscience bulletin · 2024Article
- Could mammalian inorganic polyphosphate be a crucial signaling molecule in neurological disorders?Neural regeneration research · 2024Article
- Sodium Hexametaphosphate Serves as an Inducer of Calcium Signaling.Biomolecules · 2023Article
- P2Y1 Receptor as a Catalyst of Brain Neurodegeneration.NeuroSci · 2022Review
- Endoplasmic Reticulum in Metaplasticity: From Information Processing to Synaptic Proteostasis.Molecular neurobiology · 2022Review
- Article
- Engineered Neutral Phosphorous Dendrimers Protect Mouse Cortical Neurons and Brain Organoids from Excitotoxic Death.International journal of molecular sciences · 2022Article
- Mitochondrial Inorganic Polyphosphate (polyP) Is a Potent Regulator of Mammalian Bioenergetics in SH-SY5Y Cells: A Proteomics and Metabolomics Study.Frontiers in cell and developmental biology · 2022Article
- Inorganic polyphosphate in host and microbe biology.Trends in microbiology · 2021Review
- Activation of RAGE leads to the release of glutamate from astrocytes and stimulates calcium signal in neurons.Journal of cellular physiology · 2021Article
Corrections and comments
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Authors and funding
7 authors at 4 institutions in 3 countries.
Funding
Abstract
Glutamate is one of the most important neurotransmitters in the process of signal transduction in the CNS. Excessive amounts of this neurotransmitter lead to glutamate excitotoxicity, which is accountable for neuronal death in acute neurological disorders, including stroke and trauma, and in neurodegenerative diseases. Inorganic polyphosphate (PolyP) plays multiple roles in the mammalian brain, including function as a calcium-dependent gliotransmitter mediating communication between astrocytes, while its role in the regulation of neuronal activity is unknown. Here we studied the effect of PolyP on glutamate-induced calcium signal in primary rat neurons in both physiological and pathological conditions. We found that preincubation of primary neurons with PolyP reduced glutamate-induced and AMPA-induced but not the NMDA-induced calcium signal. However, in rat hippocampal acute slices, PolyP reduced ion flux through NMDA and AMPA receptors in native neurons. The effect of PolyP on glutamate and specifically on the AMPA receptors was dependent on the presence of P2Y1 but not of P2X receptor inhibitors and also could be mimicked by P2Y1 agonist 2MeSADP. Preincubation of cortical neurons with PolyP significantly reduced the initial calcium peak as well as the number of neurons with delayed calcium deregulation in response to high concentrations of glutamate and resulted in protection of neurons against glutamate-induced cell death. As a result, activation of P2Y1 receptors by PolyP reduced calcium signal acting through AMPA receptors, thus protecting neurons against glutamate excitotoxicity by reduction of the calcium overload and restoration of mitochondrial function.
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Registered trials
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