ArticleNeurobiology of aging2018
Nonsteroidal anti-inflammatory drug, indomethacin improves spatial memory and NMDA receptor function in aged animals.
Article in Neurobiology of aging, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.
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Who cites it
21 citing papers in PubMed, 32 citations in OpenAlex.
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- The Reducing Agent Dithiothreitol Modulates the Ventilatory Responses That Occur in Freely Moving Rats during and following a Hypoxic-Hypercapnic Challenge.Antioxidants (Basel, Switzerland) · 2024Article
- Senolytic treatment alleviates doxorubicin-induced chemobrain.Aging cell · 2024Article
- Failure of senolytic treatment to prevent cognitive decline in a female rodent model of aging.Frontiers in aging neuroscience · 2024Article
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- The TgF344-AD rat: behavioral and proteomic changes associated with aging and protein expression in a transgenic rat model of Alzheimer's disease.Neurobiology of aging · 2023Article
- Naringenin Attenuates Cognitive Impairment in a Rat Model of Vascular Dementia by Inhibiting Hippocampal Oxidative Stress and Inflammatory Response and Promoting N-Methyl-D-Aspartate Receptor Signaling Pathway.Neurochemical research · 2022Article
- Transient neuroinflammation following surgery contributes to long-lasting cognitive decline in elderly rats via dysfunction of synaptic NMDA receptor.Journal of neuroinflammation · 2022Article
- Neuroinflammation as the Underlying Mechanism of Postoperative Cognitive Dysfunction and Therapeutic Strategies.Frontiers in cellular neuroscience · 2022Review
- The role of sleep disturbance and inflammation for spatial memory.Brain, behavior, & immunity - health · 2021Article
- Adulthood systemic inflammation accelerates the trajectory of age-related cognitive decline.Aging · 2021Article
- Article
- The Role of Cyclooxygenase 2 in the Cognitive Impairment Induced by Alcohol or Stress in Rats.Advanced biomedical research · 2021Article
- Differential Effect of Repeated Lipopolysaccharide Treatment and Aging on Hippocampal Function and Biomarkers of Hippocampal Senescence.Molecular neurobiology · 2020Article
- Dysregulation of BDNF/TrkB signaling mediated by NMDAR/CaJournal of neuroinflammation · 2020Article
- Senescent neurophysiology: CaNeurobiology of learning and memory · 2019Review
- Article
- Enhancement of BDNF Expression and Memory by HDAC Inhibition Requires BET Bromodomain Reader Proteins.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2019Article
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5 authors at 1 institution in 1 country.
Funding
Abstract
A redox-mediated decrease in N-methyl-D-aspartate (NMDA) receptor function contributes to psychiatric diseases and impaired cognition during aging. Inflammation provides a potential source of reactive oxygen species for inducing NMDA receptor hypofunction. The present study tested the hypothesis that the nonsteroidal anti-inflammatory drug indomethacin, which improves spatial episodic memory in aging rats, would enhance NMDA receptor function through a shift in the redox state. Male F344 young and aged rats were prescreened using a 1-day version of the water maze task. Animals were then treated with the indomethacin or vehicle, delivered in a frozen milk treat (orally, twice per day, 18 days), and retested on the water maze. Indomethacin treatment enhanced water maze performance. Hippocampal slices were prepared for examination of CA3-CA1 synaptic responses, long-term potentiation, and NMDA receptor-mediated synaptic responses. No effect of treatment was observed for the total synaptic response. Long-term potentiation magnitude and NMDA receptor input-output curves were enhanced for aged indomethacin-treated animals. To examine redox regulation of NMDA receptors, a second group of aged animals was treated with indomethacin or vehicle, and the effect of the reducing agent, dithiothreitol ([DTT], 0.5 mM) on NMDA receptor-mediated synaptic responses was evaluated. As expected, DTT increased the NMDA receptor response and the effect of DTT was reduced by indomethacin treatment. The results indicate that indomethacin acted to diminish the age-related and redox-mediated NMDA receptor hypofunction and suggest that inflammation contributes to cognitive impairment through an increase in redox stress.
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