ArticleBritish journal of pharmacology2013
Abnormal NMDA receptor function exacerbates experimental autoimmune encephalomyelitis.
Article in British journal of pharmacology, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
25 citing papers in PubMed, 46 citations in OpenAlex.
- Modulating glutamate neurotransmission inFrontiers in immunology · 2026Review
- Should We Consider Neurodegeneration by Itself or in a Triangulation with Neuroinflammation and Demyelination? The Example of Multiple Sclerosis and Beyond.International journal of molecular sciences · 2024Review
- The neuropathobiology of multiple sclerosis.Nature reviews. Neuroscience · 2024Review
- NMDA Receptor Antagonist Memantine Ameliorates Experimental Autoimmune Encephalomyelitis in Aged Rats.Biomedicines · 2024Article
- Synapse Dysfunctions in Multiple Sclerosis.International journal of molecular sciences · 2023Review
- Chronic experimental autoimmune encephalomyelitis is an excellent model to study neuroaxonal degeneration in multiple sclerosis.Frontiers in molecular neuroscience · 2022Review
- Synaptic Dysfunction in Multiple Sclerosis: A Red Thread from Inflammation to Network Disconnection.International journal of molecular sciences · 2021Review
- Neuropathic Pain in Multiple Sclerosis and Its Animal Models: Focus on Mechanisms, Knowledge Gaps and Future Directions.Frontiers in neurology · 2021Review
- Pathophysiological Ionotropic Glutamate Signalling in Neuroinflammatory Disease as a Therapeutic Target.Frontiers in neuroscience · 2021Review
- Reporting animal research: Explanation and elaboration for the ARRIVE guidelines 2.0.PLoS biology · 2020Article
- Synaptic alterations and immune response are sexually dimorphic in a non-pertussis toxin model of experimental autoimmune encephalomyelitis.Experimental neurology · 2020Article
- Enhanced GABAergic Tonic Inhibition Reduces Intrinsic Excitability of Hippocampal CA1 Pyramidal Cells in Experimental Autoimmune Encephalomyelitis.Neuroscience · 2018Article
- CaMKIIα Mediates the Effect of IL-17 To Promote Ongoing Spontaneous and Evoked Pain in Multiple Sclerosis.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2018Article
- Stem Cells as Potential Targets of Polyphenols in Multiple Sclerosis and Alzheimer's Disease.BioMed research international · 2018Review
- Interplay Between Age and Neuroinflammation in Multiple Sclerosis: Effects on Motor and Cognitive Functions.Frontiers in aging neuroscience · 2018Review
- Glutamate, T cells and multiple sclerosis.Journal of neural transmission (Vienna, Austria : 1996) · 2017Review
- Absence of system xJournal of neuroinflammation · 2017Article
- CCL5-Glutamate Cross-Talk in Astrocyte-Neuron Communication in Multiple Sclerosis.Frontiers in immunology · 2017Review
- Siponimod (BAF312) prevents synaptic neurodegeneration in experimental multiple sclerosis.Journal of neuroinflammation · 2016Article
- Synaptopathy connects inflammation and neurodegeneration in multiple sclerosis.Nature reviews. Neurology · 2015Review
Corrections and comments
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Authors and funding
18 authors at 5 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
background and purposeGlutamate transmission is dysregulated in both multiple sclerosis (MS) and experimental autoimmune encephalomyelitis (EAE), the animal model of MS. A characteristic of EAE is increased glutamate transmission associated with up-regulation of AMPA receptors. However, little is known about the role of NMDA receptors in the synaptic modifications induced by EAE. EXPERIMENTAL APPROACH: The contribution of NMDA receptors to the alterations of glutamate transmission and disease severity in EAE mice was assessed by means of neurophysiological, morphological, Western blot, metabolic and clinical score assessments. KEY
resultsIn our EAE mice, there was an NMDA receptor-dependent increase of glutamate release, associated with marked activation of the astroglia. Presynaptic NMDA receptors became overactive during EAE, increasing synaptic glutamate release by a mechanism dependent on voltage-gated sodium channels. By means of NAD(P)H autofluorescence analysis, we also found that EAE has a glutamate and NMDA receptor-dependent dysfunction of mitochondrial activity, which is known to contribute to the neurodegenerative damage of MS and EAE. Furthermore, pharmacological blockade of NMDA receptors in vivo ameliorated both synaptic transmission defects and of the clinical disease course of EAE mice, while EAE induced in mice with a genetically enhanced NMDA receptor signalling had opposite effects. CONCLUSIONS AND IMPLICATIONS: Our data, showing both sensitization of NMDA receptors and their involvement in the progression of the EAE disease, supggest that pharmacological impairment of NMDA receptor signalling would be a component of a neuroprotection strategy in MS.
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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.