ArticleFree radical biology & medicine2010
Long-lasting inhibition of presynaptic metabolism and neurotransmitter release by protein S-nitrosylation.
Article in Free radical biology & medicine, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.
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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
19 citing papers in PubMed, 30 citations in OpenAlex.
- NOX-NOS crosstalk in the liver-brain axis: Novel insights for redox regulation and neurodegenerative diseases.Redox biology · 2025Review
- Hypoxia releases S-nitrosocysteine from carotid body glomus cells-relevance to expression of the hypoxic ventilatory response.Frontiers in pharmacology · 2023Article
- S-nitroso-L-cysteine stereoselectively blunts the adverse effects of morphine on breathing and arterial blood gas chemistry while promoting analgesia.Biomedicine & pharmacotherapy = Biomedecine & pharmacotherapie · 2022Article
- Adherence to a Mediterranean Diet Is Associated with Lower Depressive Symptoms among U.S. Adults.Nutrients · 2022Article
- S-Nitroso-L-Cysteine Stereoselectively Blunts the Deleterious Effects of Fentanyl on Breathing While Augmenting Antinociception in Freely-Moving Rats.Frontiers in pharmacology · 2022Article
- Neuromeric Distribution of Nicotinamide Adenine Dinucleotide Phosphate-Diaphorase Activity in the Adult Lamprey Brain.Frontiers in neuroanatomy · 2022Article
- Reactive Oxygen Species: Beyond Their Reactive Behavior.Neurochemical research · 2021Review
- Mechanisms of soft and hard electrophile toxicities.Toxicology · 2019Review
- Redox Signaling in Neurotransmission and Cognition During Aging.Antioxidants & redox signaling · 2018Review
- Endogenous nitric oxide inhibits spinal NMDA receptor activity and pain hypersensitivity induced by nerve injury.Neuropharmacology · 2017Article
- Nitric Oxide-Mediated Posttranslational Modifications: Impacts at the Synapse.Oxidative medicine and cellular longevity · 2016Review
- The neuroprotective properties of the superoxide dismutase mimetic tempol correlate with its ability to reduce pathological glutamate release in a rodent model of stroke.Free radical biology & medicine · 2014Article
- Dual effect of exogenous nitric oxide on neuronal excitability in rat substantia gelatinosa neurons.Neural plasticity · 2014Article
- Inhibition of autophagy and glycolysis by nitric oxide during hypoxia-reoxygenation impairs cellular bioenergetics and promotes cell death in primary neurons.Free radical biology & medicine · 2013Article
- S-nitrosothiols and the S-nitrosoproteome of the cardiovascular system.Antioxidants & redox signaling · 2013Review
- DCPIB, the proposed selective blocker of volume-regulated anion channels, inhibits several glutamate transport pathways in glial cells.Molecular pharmacology · 2013Article
- Molecular mechanism of acrylamide neurotoxicity: lessons learned from organic chemistry.Environmental health perspectives · 2012Review
- Selective vulnerability of synaptic signaling and metabolism to nitrosative stress.Antioxidants & redox signaling · 2012Review
- Nitric oxide inhibits nociceptive transmission by differentially regulating glutamate and glycine release to spinal dorsal horn neurons.The Journal of biological chemistry · 2011Article
Corrections and comments
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Authors and funding
6 authors at 1 institution in 1 country.
Funding
Abstract
Nitric oxide (NO) and related reactive nitrogen species (RNS) play a major role in the pathophysiology of stroke and other neurodegenerative diseases. One of the poorly understood consequences of stroke is a long-lasting inhibition of synaptic transmission. In this study, we tested the hypothesis that RNS can produce long-term inhibition of neurotransmitter release via S-nitrosylation of proteins in presynaptic nerve endings. We examined the effects of exogenous sources of RNS on the vesicular and nonvesicular L-[(3)H]glutamate release from rat brain synaptosomes. NO/RNS donors, such as spermine NONOate, MAHMA NONOate, S-nitroso-L-cysteine, and SIN-1, inhibited only the vesicular component of glutamate release with an order of potency that closely matched levels of protein S-nitrosylation. Inhibition of glutamate release persisted for >1h after RNS donor decomposition and washout and strongly correlated with decreases in the intrasynaptosomal ATP levels. Post-NO treatment of synaptosomes with thiol-reducing reagents decreased the total content of S-nitrosylated proteins but had little effect on glutamate release and ATP levels. In contrast, post-NO application of the end-product of glycolysis, pyruvate, partially rescued neurotransmitter release and ATP production. These data suggest that RNS suppress presynaptic metabolism and neurotransmitter release via poorly reversible modifications of glycolytic and mitochondrial enzymes, one of which was identified as glyceraldehyde-3-phosphate dehydrogenase. A similar mechanism may contribute to the long-term suppression of neuronal communication during nitrosative stress in vivo.
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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.