ArticleThe Journal of neuroscience : the official journal of the Society for Neuroscience2013
Linking redox regulation of NMDAR synaptic function to cognitive decline during aging.
Article in The Journal of neuroscience : the official journal of the Society for Neuroscience, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 54 papers.
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Who cites it
54 citing papers in PubMed, 76 citations in OpenAlex.
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- Failure of senolytic treatment to prevent cognitive decline in a female rodent model of aging.Frontiers in aging neuroscience · 2024Article
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- Modulation of Hippocampal Astroglial Activity by Synaptamide in Rats with Neuropathic Pain.Brain sciences · 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
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- Targeting redox-altered plasticity to reactivate synaptic function: A novel therapeutic strategy for cognitive disorder.Acta pharmaceutica Sinica. B · 2021Review
- Effects of Aging on the Structure and Expression of NMDA Receptors of Somatostatin Expressing Neurons in the Mouse Hippocampus.Frontiers in aging neuroscience · 2021Article
- Cognitive Impact by Blood Circulating Anti-NMDAR1 Autoantibodies.Journal of psychiatry and brain science · 2021Article
- Differential Effect of Repeated Lipopolysaccharide Treatment and Aging on Hippocampal Function and Biomarkers of Hippocampal Senescence.Molecular neurobiology · 2020Article
Corrections and comments
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Authors and funding
2 authors at 1 institution in 1 country.
Funding
Abstract
NMDA receptors (NMDARs) play a critical role in learning and memory; however, there is a lack of evidence for a direct relationship between a well characterized decline in NMDAR function and impaired cognition during aging. The present study was designed to test the idea that a redox-mediated decrease in the NMDAR component of synaptic transmission during aging is related to a specific cognitive phenotype: impaired memory for rapidly acquired novel spatial information. Young and middle-aged male F344 rats were provided 1 d of training on the spatial version of the water maze, and retention was examined 24 h later. The performance of young rats was used as a criterion for classifying middle-aged rats as impaired and unimpaired on the task. Subsequent construction of CA3-CA1 synaptic input-output curves in hippocampal slices confirmed an age-related decrease in synaptic responses, including the NMDAR component of synaptic transmission. Examination of synaptic transmission according to behavioral classification revealed that animals classified as impaired exhibited a decrease in the total and the NMDAR component of the synaptic response relative to unimpaired animals. Furthermore, bath application of the reducing agent dithiothreitol increased the NMDAR component of the synaptic response to a greater extent in impaired animals relative to unimpaired and young rats. These results provide evidence for a link between the redox-mediated decline in NMDAR function and emergence of an age-related cognitive phenotype, impairment in the rapid acquisition and retention of novel spatial information.
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