ArticleNeurobiology of aging2014
Role of antioxidant enzymes in redox regulation of N-methyl-D-aspartate receptor function and memory in middle-aged rats.
Article in Neurobiology of aging, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.
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Who cites it
20 citing papers in PubMed, 36 citations in OpenAlex.
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- The Role of PKC in Regulating NMDARs in Aluminum-Induced Learning and Memory Impairment in Rats.Neurotoxicity research · 2021Article
- Adulthood systemic inflammation accelerates the trajectory of age-related cognitive decline.Aging · 2021Article
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- Senescent neurophysiology: CaNeurobiology of learning and memory · 2019Review
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- Alteration in NMDA Receptor Mediated Glutamatergic Neurotransmission in the Hippocampus During Senescence.Neurochemical research · 2019Review
- Nonsteroidal anti-inflammatory drug, indomethacin improves spatial memory and NMDA receptor function in aged animals.Neurobiology of aging · 2018Article
- Redox Signaling in Neurotransmission and Cognition During Aging.Antioxidants & redox signaling · 2018Review
- The role of air pollution in myocardial remodeling.PloS one · 2017Article
- Preclinical Magnetic Resonance Imaging and Spectroscopy Studies of Memory, Aging, and Cognitive Decline.Frontiers in aging neuroscience · 2016Review
- Re-Opening the Critical Window for Estrogen Therapy.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2015Article
- Contribution of N-methyl-D-aspartate receptors to attention and episodic spatial memory during senescence.Neurobiology of learning and memory · 2015Article
- Impaired attention and synaptic senescence of the prefrontal cortex involves redox regulation of NMDA receptors.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2015Article
- Behavioral and Neurochemical Deficits in Aging Rats with Increased Neonatal Iron Intake: Silibinin's Neuroprotection by Maintaining Redox Balance.Frontiers in aging neuroscience · 2015Article
- Age-related deficits in synaptic plasticity rescued by activating PKA or PKC in sensory neurons of Aplysia californica.Frontiers in aging neuroscience · 2015Article
- NMDA Receptor Function During Senescence: Implication on Cognitive Performance.Frontiers in neuroscience · 2015Review
- Targeting multiple pathogenic mechanisms with polyphenols for the treatment of Alzheimer's disease-experimental approach and therapeutic implications.Frontiers in aging neuroscience · 2014Article
Corrections and comments
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Authors and funding
4 authors at 2 institutions in 1 country.
Funding
Abstract
Overexpression of superoxide dismutase 1 (SOD1) in the hippocampus results in age-dependent impaired cognition and altered synaptic plasticity suggesting a possible model for examining the role of oxidative stress in senescent neurophysiology. However, it is unclear if SOD1 overexpression involves an altered redox environment and a decrease in N-methyl-D-aspartate receptor (NMDAR) synaptic function reported for aging animals. Viral vectors were used to express SOD1 and green fluorescent protein (SOD1 + GFP), SOD1 and catalase (SOD1 + CAT), or GFP alone in the hippocampus of middle-aged (17 months) male Fischer 344 rats. We confirm that SOD1 + GFP and SOD1 + CAT reduced lipid peroxidation indicating superoxide metabolites were primarily responsible for lipid peroxidation. SOD1 + GFP impaired learning, decreased glutathione peroxidase activity, decreased glutathione levels, decreased NMDAR-mediated synaptic responses, and impaired long-term potentiation. Co-expression of SOD1 + CAT rescued the effects of SOD1 expression on learning, redox measures, and synaptic function suggesting the effects were mediated by excess hydrogen peroxide. Application of the reducing agent dithiolthreitol to hippocampal slices increased the NMDAR-mediated component of the synaptic response in SOD1 + GFP animals relative to animals that overexpress SOD1 + CAT indicating that the effect of antioxidant enzyme expression on NMDAR function was because of a shift in the redox environment. The results suggest that overexpression of neuronal SOD1 and CAT in middle age may provide a model for examining the role of oxidative stress in senescent physiology and the progression of age-related neurodegenerative 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.