ArticleThe Journal of neuroscience : the official journal of the Society for Neuroscience1997
Mechanisms of cell death induced by the mitochondrial toxin 3-nitropropionic acid: acute excitotoxic necrosis and delayed apoptosis.
Article in The Journal of neuroscience : the official journal of the Society for Neuroscience, 1997. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 45 papers.
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Who cites it
45 citing papers in PubMed, 248 citations in OpenAlex.
- Neuroinflammation in Huntington's Disease: A Starring Role for Astrocyte and Microglia.Current neuropharmacology · 2022Review
- A Rationale for Hypoxic and Chemical Conditioning in Huntington's Disease.International journal of molecular sciences · 2021Review
- Genes to treat excitotoxicity ameliorate the symptoms of the disease in mice models of multiple system atrophy.Journal of neural transmission (Vienna, Austria : 1996) · 2020Article
- Lack of PINK1 alters glia innate immune responses and enhances inflammation-induced, nitric oxide-mediated neuron death.Scientific reports · 2018Article
- Rutin as a Potent Antioxidant: Implications for Neurodegenerative Disorders.Oxidative medicine and cellular longevity · 2018Review
- N-Adamantyl-4-Methylthiazol-2-Amine Attenuates Glutamate-Induced Oxidative Stress and Inflammation in the Brain.Neurotoxicity research · 2017Article
- An E3-ligase-based method for ablating inhibitory synapses.Nature methods · 2016Article
- Increased Expression of Osteopontin in the Degenerating Striatum of Rats Treated with Mitochondrial Toxin 3-Nitropropionic Acid: A Light and Electron Microscopy Study.Acta histochemica et cytochemica · 2015Article
- Mitochondrial succinate dehydrogenase is involved in stimulus-secretion coupling and endogenous ROS formation in murine beta cells.Diabetologia · 2015Article
- 3-Nitropropionic acid induces ovarian oxidative stress and impairs follicle in mouse.PloS one · 2014Article
- Ginseng ginsenoside pharmacology in the nervous system: involvement in the regulation of ion channels and receptors.Frontiers in physiology · 2014Review
- Autophagy and neuronal cell death in neurological disorders.Cold Spring Harbor perspectives in biology · 2012Review
- Brief mitochondrial inhibition causes lasting changes in motor behavior and corticostriatal synaptic physiology in the Fischer 344 rat.Neuroscience · 2012Article
- PINK1 enhances insulin-like growth factor-1-dependent Akt signaling and protection against apoptosis.Neurobiology of disease · 2012Article
- Induction of Apoptosis in Human Leukemia Cell Line (HL60) by Animal's Venom Derived Peptides (ICD-85).Iranian journal of pharmaceutical research : IJPR · 2012Article
- Review
- Acetyl-L-Carnitine Modulates TP53 and IL10 Gene Expression Induced by 3-NPA Evoked Toxicity in PC12 Cells.Current neuropharmacology · 2011Article
- Chronic ethanol consumption enhances sensitivity to Ca(2+)-mediated opening of the mitochondrial permeability transition pore and increases cyclophilin D in liver.American journal of physiology. Gastrointestinal and liver physiology · 2010Article
- Ketones prevent synaptic dysfunction induced by mitochondrial respiratory complex inhibitors.Journal of neurochemistry · 2010Article
- Lactoferrin decreases LPS-induced mitochondrial dysfunction in cultured cells and in animal endotoxemia model.Innate immunity · 2010Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
2 authors at 1 institution in 1 country.
Funding
Abstract
Impaired energy metabolism may play an important role in neuronal cell death after brain ischemia and in late-onset neurodegenerative diseases. Both excitotoxic necrosis and apoptosis have been implicated in cell death induced by metabolic impairment. However, the factors that determine whether cells undergo apoptosis or necrosis are not known. In the present study, metabolic impairment was induced by 3-nitropropionic acid (3-NP), a suicide inhibitor of succinate dehydrogenase. Treatment of cultured rat hippocampal neurons with 3-NP resulted in two types of cell death with distinct morphological, pharmacological, and biochemical features. A rapid necrotic cell death, characterized by cell swelling and nuclear shrinkage, could be completely prevented by the NMDA receptor antagonist MK-801 (10 microM) and dose-dependently potentiated by low micromolar levels of extracellular glutamate. A slowly evolving apoptotic death, characterized by nuclear fragmentation, was not attenuated by MK-801 but was prevented by cycloheximide (1 microg/ml). The combination of MK-801 and cycloheximide resulted in an almost complete protection against 3-NP-induced cell death. DNA fragmentation, detected by the terminal deoxynucleotidyl transferase-mediated dUTP-X 3' nick end-labeling technique, was a late event in apoptosis and also occurred after necrotic cell death. ATP depletion was an early event in the 3-NP-induced neuronal degeneration, and the decline in ATP was exacerbated by glutamate. We conclude that 3-NP triggers two separate cell death pathways: an excitotoxic necrosis as a result of NMDA receptor activation and a delayed apoptosis that is NMDA receptor-independent. Mildly elevated levels of extracellular glutamate shift the cell death mechanism from apoptosis to necrosis.
Indexed as
Identifiers
9096141PMC6573656W2145413598What OpenQuestion holds
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.