ArticleAging2019
Subunit contribution to NMDA receptor hypofunction and redox sensitivity of hippocampal synaptic transmission during aging.
Article in Aging, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 papers, 1 of them a synthesis that pooled it.
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
27 citing papers in PubMed, 1 synthesis or guideline pooled it, 39 citations in OpenAlex.
- Neuronal surface autoantibodies in dementia: a systematic review and meta-analysis.Journal of neurology · 2021Pooled it
- Revisiting ROS: duality in organ aging progression.Molecular biology reports · 2025Review
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- Sex, senescence, senolytics, and cognition.Frontiers in aging neuroscience · 2025Review
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- Senolytic treatment alleviates doxorubicin-induced chemobrain.Aging cell · 2024Article
- Mapping hippocampal glutamate in healthy aging withFrontiers in aging neuroscience · 2024Article
- Neuronal Senescence in the Aged Brain.Aging and disease · 2023Review
- Article
- Article
- A Consequence of Immature Breathing induces Persistent Changes in Hippocampal Synaptic Plasticity and Behavior: A Role of Pro-Oxidant State and NMDA Receptor Imbalance.bioRxiv : the preprint server for biology · 2023Article
- Age-related changes in excitatory and inhibitory intra-cortical circuits in auditory cortex of C57Bl/6 mice.Hearing research · 2023Article
- Nicotinic acetylcholine receptors and learning and memory deficits in Neuroinflammatory diseases.Frontiers in neuroscience · 2023Review
- N-methyl-D-aspartate receptor hypofunction as a potential contributor to the progression and manifestation of many neurological disorders.Frontiers in molecular neuroscience · 2023Review
- A consequence of immature breathing induces persistent changes in hippocampal synaptic plasticity and behavior: a role of prooxidant state and NMDA receptor imbalance.Frontiers in molecular neuroscience · 2023Article
- NX210c Peptide Promotes Glutamatergic Receptor-Mediated Synaptic Transmission and Signaling in the Mouse Central Nervous System.International journal of molecular sciences · 2022Article
- Altered Metabolism in Alzheimer Disease Brain: Role of Oxidative Stress.Antioxidants & redox signaling · 2022Review
- Altered Response Dynamics and Increased Population Correlation to Tonal Stimuli Embedded in Noise in Aging Auditory Cortex.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2021Article
- Intermittent Hypoxia causes targeted disruption to NMDA receptor dependent synaptic plasticity in area CA1 of the hippocampus.Experimental neurology · 2021Article
- Adulthood systemic inflammation accelerates the trajectory of age-related cognitive decline.Aging · 2021Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
3 authors at 1 institution in 1 country.
Funding
Abstract
We examined the contribution of N-methyl-D-aspartate receptor (NMDAR) subunits in the redox-mediated decline in NMDAR function during aging. GluN2A and GluN2B selective antagonists decreased peak NMDAR currents to a similar extent in young and aged animals, indicating that a shift in diheteromeric GluN2 subunits does not underlie the age-related decrease in the NMDAR synaptic function. Application of dithiothreitol (DTT) in aged animals, increased peak NMDAR synaptic currents, prolonged the decay time, and increased the sensitivity of the synaptic response to the GluN2B antagonist, ifenprodil, indicating that DTT increased the contribution of GluN2B subunits to the synaptic response. The DTT-mediated increase in NMDAR function was inhibited by partial blockade of NMDARs, and this inhibition was rescued by increasing Ca
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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.