ArticleNeuroscience2011
Exposure of neurons to excitotoxic levels of glutamate induces cleavage of the RNA editing enzyme, adenosine deaminase acting on RNA 2, and loss of GLUR2 editing.
Article in Neuroscience, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers, 1 of them a synthesis that pooled it.
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Who cites it
23 citing papers in PubMed, 1 synthesis or guideline pooled it, 41 citations in OpenAlex.
- Research Progress on the Antidepressant Effects of Baicalin and Its Aglycone Baicalein: A Systematic Review of the Biological Mechanisms.Neurochemical research · 2024Pooled it
- Implications for soluble iron accumulation, oxidative stress, and glial glutamate release in motor neuron death associated with sporadic amyotrophic lateral sclerosis.Neuropathology : official journal of the Japanese Society of Neuropathology · 2025Review
- Regulation of microglial responses after pediatric traumatic brain injury: exploring the role of SHIP-1.Frontiers in neuroscience · 2023Article
- The role of PI3K-mediated AMPA receptor changes in post-conditioning of propofol in brain protection.BMC neuroscience · 2019Article
- ADAR2-mediated Q/R editing of GluK2 regulates kainate receptor upscaling in response to suppression of synaptic activity.Journal of cell science · 2018Article
- Tinospora cordifolia as a potential neuroregenerative candidate against glutamate induced excitotoxicity: an in vitro perspective.BMC complementary and alternative medicine · 2018Article
- Synaptic dysfunction and altered excitability in C9ORF72 ALS/FTD.Brain research · 2018Review
- ADAR RNA editing in human disease; more to it than meets the I.Human genetics · 2017Review
- Evaluating a Gene-Environment Interaction in Amyotrophic Lateral Sclerosis: Methylmercury Exposure and Mutated SOD1.Current environmental health reports · 2017Review
- Neuropathic pain promotes adaptive changes in gene expression in brain networks involved in stress and depression.Science signaling · 2017Article
- EAAT2 and the Molecular Signature of Amyotrophic Lateral Sclerosis.Advances in neurobiology · 2017Review
- Review
- Glial TDP-43 regulates axon wrapping, GluRIIA clustering and fly motility by autonomous and non-autonomous mechanisms.Human molecular genetics · 2015Article
- Regulatory factors governing adenosine-to-inosine (A-to-I) RNA editing.Bioscience reports · 2015Review
- Chronic glutamate treatment selectively modulates AMPA RNA editing and ADAR expression and activity in primary cortical neurons.RNA biology · 2015Article
- Advances in cellular models to explore the pathophysiology of amyotrophic lateral sclerosis.Molecular neurobiology · 2014Review
- Calcium-permeable AMPA receptors in neonatal hypoxic-ischemic encephalopathy (Review).Biomedical reports · 2013Article
- Synergistic inhibition of survival, proliferation, and migration of U87 cells with a combination of LY341495 and Iressa.PloS one · 2013Article
- Activity regulation of adenosine deaminases acting on RNA (ADARs).Molecular neurobiology · 2012Review
- The essential role of AMPA receptor GluR2 subunit RNA editing in the normal and diseased brain.Frontiers in molecular neuroscience · 2012Article
Corrections and comments
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Authors and funding
4 authors at 2 institutions in 2 countries.
Funding
Abstract
AMPA receptors are glutamate receptors that are tetramers of various combinations of GluR1-4 subunits. AMPA receptors containing GluR1, 3 and 4 are Ca2+ permeable, however, AMPA receptors containing even a single subunit of GluR2 are Ca2+ impermeable. Most AMPA receptors are Ca2+ impermeable due to the presence of GluR2. GluR2 confers special properties on AMPA receptors through the presence of arginine at the pore apex; other subunits (GluR1, 3, 4) contain glutamine at the pore apex and allow Ca2+ influx. Normally, an RNA editing step changes DNA-encoded glutamine to arginine, introduces arginine in the GluR2 pore apex. GluR2 RNA editing is carried out by an RNA-dependent adenosine deaminase (ADAR2). Loss of GluR2 editing leads to the formation of highly excitotoxic AMPA channels [Mahajan and Ziff (2007) Mol Cell Neurosci 35:470-481] and is shown to contribute to loss of motor neurons in amyotrophic lateral sclerosis (ALS). Relatively higher levels of Ca2+-permeable AMPA receptors are found in motor neurons and this has been correlated with lower GluR2 mRNA levels. However, the reason for loss of GluR2 editing is not known. Here we show that exposure of neurons to excitotoxic levels of glutamate leads to specific cleavage of ADAR2 that leads to generation of unedited GluR2. We demonstrate that cleaved ADAR2 leads to a decrease or loss of GluR2 editing, which will further result in high Ca2+ influx and excitotoxic neuronal death.
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Registered trials
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.