ReviewMolecular neurobiology2013
Oligodendrocyte N-methyl-D-aspartate receptor signaling: insights into its functions.
Review in Molecular neurobiology, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
What it found
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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
9 citing papers in PubMed, 15 citations in OpenAlex.
- Excitotoxic Storms of Ischemic Stroke: A Non-neuronal Perspective.Molecular neurobiology · 2024Review
- NMDARs in Alzheimer's Disease: Between Synaptic and Extrasynaptic Membranes.International journal of molecular sciences · 2024Review
- Caught in vicious circles: a perspective on dynamic feed-forward loops driving oxidative stress in schizophrenia.Molecular psychiatry · 2022Review
- Linking proteomic alterations in schizophrenia hippocampus to NMDAr hypofunction in human neurons and oligodendrocytes.European archives of psychiatry and clinical neuroscience · 2021Article
- In vivo spatiotemporal patterns of oligodendrocyte and myelin damage at the neural electrode interface.Biomaterials · 2021Article
- Src Family Kinases Inhibition Ameliorates Hypoxic-Ischemic Brain Injury in Immature Rats.Frontiers in cellular neuroscience · 2021Article
- D-Aspartate treatment attenuates myelin damage and stimulates myelin repair.EMBO molecular medicine · 2019Article
- Redox dysregulation, neuroinflammation, and NMDA receptor hypofunction: A "central hub" in schizophrenia pathophysiology?Schizophrenia research · 2016Review
- Effect of MK-801 and Clozapine on the Proteome of Cultured Human Oligodendrocytes.Frontiers in cellular neuroscience · 2016Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
2 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Myelination by oligodendrocytes facilitates rapid nerve conduction. Loss of oligodendrocytes and failure of myelination lead to nerve degeneration and numerous demyelinating white matter diseases. N-methyl-D-aspartate (NMDA) receptors, which are key regulators on neuron survival and functions, have been recently identified to express in oligodendrocytes, especially in the myelin sheath. NMDA receptor signaling in oligodendrocytes plays crucial roles in energy metabolism and myelination. In the present review, we highlight the subcellular location-specific impairment of excessive NMDA receptor signaling on oligodendrocyte energy metabolism in soma and myelin, and the mechanisms including Ca(2+) overload, acidotoxicity, mitochondria dysfunction, and impairment of respiratory chains. Conversely, physiological NMDA receptor signaling regulates differentiation and migration of oligodendrocytes. How can we use above knowledge to treat excitotoxic oligodendrocyte loss, congenital myelination deficiency, or postnatal demyelination? A thorough understanding of NMDA receptor signaling-mediated cellular events in oligodendrocytes at the pathophysiological level will no doubt aid in exploring effective therapeutic strategies for demyelinating white matter diseases.
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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.