ArticleNeuroscience letters2010
Neuroprotective effects of pyruvate following NMDA-mediated excitotoxic insults in hippocampal slices.
Article in Neuroscience letters, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.
What it found
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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.
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Who cites it
23 citing papers in PubMed, 31 citations in OpenAlex.
- Multitargeted Neuroprotective Strategies of Ethyl Pyruvate: From Molecular Mechanisms to Clinical Perspectives in CNS Disorders.Biomolecules & therapeutics · 2026Review
- Glutamate, NAA, and energy metabolism in clinical high risk and first episode psychosis.Scientific reports · 2025Article
- The Role of Mitochondrial Pyruvate Carrier in Neurological Disorders.Molecular neurobiology · 2025Review
- Additive aluminum as a cause of induced immunoexcitoxicity resulting in neurodevelopmental and neurodegenerative disorders: A biochemical, pathophysiological, and pharmacological analysis.Surgical neurology international · 2024Article
- The mitochondrial pyruvate carrier at the crossroads of intermediary metabolism.American journal of physiology. Endocrinology and metabolism · 2022Review
- Alternative substrate metabolism depends on cerebral metabolic state following traumatic brain injury.Experimental neurology · 2020Article
- Targeting the Mitochondrial Pyruvate Carrier for Neuroprotection.Brain sciences · 2019Review
- 'SNO'-Storms Compromise Protein Activity and Mitochondrial Metabolism in Neurodegenerative Disorders.Trends in endocrinology and metabolism: TEM · 2017Review
- Affected energy metabolism under manganese stress governs cellular toxicity.Scientific reports · 2017Article
- Nitric Oxide Synthase-2-Derived Nitric Oxide Drives Multiple Pathways of Breast Cancer Progression.Antioxidants & redox signaling · 2017Review
- Parkinson's disease: Microglial/macrophage-induced immunoexcitotoxicity as a central mechanism of neurodegeneration.Surgical neurology international · 2017Review
- Robust neuroprotective effects of 2-((2-oxopropanoyl)oxy)-4-(trifluoromethyl)benzoic acid (OPTBA), a HTB/pyruvate ester, in the postischemic rat brain.Scientific reports · 2016Article
- Pyruvate treatment attenuates cerebral metabolic depression and neuronal loss after experimental traumatic brain injury.Brain research · 2016Article
- L-Lactate protects neurons against excitotoxicity: implication of an ATP-mediated signaling cascade.Scientific reports · 2016Article
- Metabolic Dysfunctions in Amyotrophic Lateral Sclerosis Pathogenesis and Potential Metabolic Treatments.Frontiers in neuroscience · 2016Review
- Degeneration of spinal motor neurons by chronic AMPA-induced excitotoxicity in vivo and protection by energy substrates.Acta neuropathologica communications · 2015Article
- Energy substrates protect hippocampus against endogenous glutamate-mediated neurodegeneration in awake rats.Neurochemical research · 2014Article
- The pathophysiology of traumatic brain injury at a glance.Disease models & mechanisms · 2013Article
- NMDA receptors and metaplasticity: mechanisms and possible roles in neuropsychiatric disorders.Neuroscience and biobehavioral reviews · 2012Review
- Adaptation of microplate-based respirometry for hippocampal slices and analysis of respiratory capacity.Journal of neuroscience research · 2011Article
Corrections and comments
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Authors and funding
2 authors at 1 institution in 1 country.
Funding
Abstract
The activation of N-methyl-D-aspartate (NMDA) receptors and subsequent release of nitric oxide (NO) are likely contributors to the delayed neuronal damage that accompanies ischemia and other neurodegenerative conditions. NMDA receptor antagonists and inhibitors of NO synthesis, however, are of limited benefit when administered following excitotoxic events, suggesting the importance of determining downstream events that result in neuronal degeneration. Inhibition of glyceraldehyde-3-phosphate-dehydrogenase (GAPDH), a key glycolytic enzyme, which may result in glycolytic impairment, is one of the biological targets of NO. This suggests that alternative energy substrates may prevent neuronal damage. Using rat hippocampal slices from juvenile rats, we examined the role of glycolytic impairment in NMDA-mediated excitotoxicity and whether pyruvate, an end product of glycolysis, prevents the excitotoxic neuronal injury. We observed that administration of NMDA acutely depresses ATP levels and result in a slowly developing inhibition of GAPDH. Unlike NMDA receptor antagonists or NO inhibitors, exogenously applied pyruvate is effective in restoring ATP levels and preventing delayed neuronal degeneration and synaptic deterioration when administered in the period following NMDA receptor activation. This raises the possibility that treatment with agents that maintain cellular energy function can prevent delayed excitotoxicity.
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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.