ReviewBiochemical Society transactions2009
Coupling of the NMDA receptor to neuroprotective and neurodestructive events.
Review in Biochemical Society transactions, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 134 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
134 citing papers in PubMed, 258 citations in OpenAlex.
- Trial
- Aberrant protein S-nitrosylation disrupts axonal development and metabolic homeostasis in a Cntnap2 mouse model of autism.Redox biology · 2026Article
- Metabolic Competition Between Microglia and Neurons as Driver of Chronic Pain.Molecular neurobiology · 2026Review
- Proteolytic cleavage of G3BP1 by calpain 1 couples NMDAR activation to mTOR-dependent local translation.EMBO reports · 2026Article
- Synaptic control of retinal ganglion cell survival and axon regeneration.Molecular neurodegeneration · 2026Review
- Exploring NMDAR pathways in ischemic stroke: implications for neurotoxic and neuroprotective mechanisms and therapeutic strategies.Naunyn-Schmiedeberg's archives of pharmacology · 2025Review
- Biological Plausibility of Using Plasma Amino Acid Profile Determination as a Potential Biomarker for Pediatric Patients with Mild Traumatic Brain Injuries.Neurology international · 2025Article
- Early involvement of D-serine in β-amyloid-dependent pathophysiology.Cellular and molecular life sciences : CMLS · 2025Article
- A genetically encoded secreted toxin potentiates synaptic NMDA receptors in hippocampal neurons and confers neuroprotection.PNAS nexus · 2025Article
- Dose-Dependent Modulation of NMDA Receptors: Neuroprotective Mechanisms against Oxidative Stress in Hippocampal Neurons.International journal of molecular and cellular medicine · 2025Article
- Article
- Discovery of novel positive allosteric modulators targeting GluN1/2A NMDARs as anti-stroke therapeutic agents.RSC medicinal chemistry · 2024Article
- Rhoa/ROCK, mTOR and Secretome-Based Treatments for Ischemic Stroke: New Perspectives.Current issues in molecular biology · 2024Review
- Exploring Ciprofol Alternatives: A Comprehensive Review of Intravenous Anesthesia Options.Cureus · 2024Review
- The Research Progress of Mitochondrial Transplantation in the Treatment of Mitochondrial Defective Diseases.International journal of molecular sciences · 2024Review
- Revisiting the calpain hypothesis of learning and memory 40 years later.Frontiers in molecular neuroscience · 2024Review
- Therapeutic Potential of Capsaicin in Various Neurodegenerative Diseases with Special Focus on Nrf2 Signaling.Current pharmaceutical biotechnology · 2024Review
- The GluN2B-Containing NMDA Receptor Alleviates Neuronal Apoptosis in Neonatal Hypoxic-Ischemic Encephalopathy by Activating PI3K-Akt-CREB Signaling Pathwa.Physiological research · 2023Article
- Smouldering Lesion in MS: Microglia, Lymphocytes and Pathobiochemical Mechanisms.International journal of molecular sciences · 2023Review
- Article
74 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
1 author at 1 institution in 1 country.
Funding
Abstract
NMDA (N-methyl-D-aspartate) receptors are a subtype of ionotropic glutamate receptor with an important role in the physiology and pathophysiology of central neurons. Inappropriate levels of Ca(2+) influx through the NMDA receptor can contribute to neuronal loss in acute trauma such as ischaemia and traumatic brain injury, as well as certain neurodegenerative diseases such as Huntington's disease. However, normal physiological patterns of NMDA receptor activity can promote neuroprotection against both apoptotic and excitotoxic insults. As a result, NMDA receptor blockade can promote neuronal death outright or render neurons vulnerable to secondary trauma. Thus responses to NMDA receptor activity follow a classical hormetic dose-response curve: both too much and too little can be harmful. There is a growing knowledge of the molecular mechanisms underlying both the neuroprotective and neurodestructive effects of NMDA receptor activity, as well as the factors that determine whether an episode of NMDA receptor activity is harmful or beneficial. It is becoming apparent that oxidative stress plays a role in promoting neuronal death in response to both hyper- and hypo-activity of the NMDA receptor. Increased understanding in this field is leading to the discovery of new therapeutic targets and strategies for excitotoxic disorders, as well as a growing appreciation of the harmful consequences of NMDA receptor blockade.
Indexed as
Identifiers
What OpenQuestion holds
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.