ArticleJournal of neuroscience research2009
Contribution of a mitochondrial pathway to excitotoxic neuronal necrosis.
Article in Journal of neuroscience research, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 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
10 citing papers in PubMed, 21 citations in OpenAlex.
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- Down-regulation of Pin1 in Temporal Lobe Epilepsy Patients and Mouse Model.Neurochemical research · 2017Article
- NR4A1 Knockdown Suppresses Seizure Activity by Regulating Surface Expression of NR2B.Scientific reports · 2016Article
- Rapid surface accumulation of NMDA receptors increases glutamatergic excitation during status epilepticus.Neurobiology of disease · 2013Article
- α-Synuclein protects neurons from apoptosis downstream of free-radical production through modulation of the MAPK signalling pathway.Neurotoxicity research · 2013Article
- Distinct caspase pathways mediate necrosis and apoptosis in subpopulations of hippocampal neurons after status epilepticus.Epilepsia · 2010Article
- Vulnerability of postnatal hippocampal neurons to seizures varies regionally with their maturational stage.Neurobiology of disease · 2010Article
Corrections and comments
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Authors and funding
5 authors at 3 institutions in 2 countries.
Funding
Abstract
It is traditionally thought that excitotoxic necrosis is a passive mechanism that does not require the activation of a cell death program. In this study, we examined the contribution of the cytochrome c-dependent mitochondrial death pathway to excitotoxic neuronal necrosis, induced by exposing cultured cortical neurons to 1 mM glutamate for 6 hr and blocked by the NMDA antagonist, dizocilpine. Glutamate treatment induced early cytochrome c release, followed by activation of caspase-9 and caspase-3. Preincubation with the caspase-9 inhibitor z-LEHD-fmk, the caspase-3 inhibitor z-DEVD-fmk, or the specific pan-caspase inhibitor Q-VD-oph decreased the percentage of propidium iodide-positive neurons (52.5% +/- 3.1%, 39.4% +/- 3.5%, 44.6% +/- 3%, respectively, vs. 65% +/- 3% in glutamate + vehicle). EM studies showed mitochondrial release of cytochrome c in neurons in the early stages of necrosis and cleaved caspase-3 immunoreactivity in morphologically necrotic neurons. These results suggest that an active mechanism contributes to the demise of a subpopulation of excitotoxic necrotic neurons.
Indexed as
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What 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.