ReviewMolecular neurobiology2010
Changes in brain cholesterol metabolome after excitotoxicity.
Review in Molecular neurobiology, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 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
20 citing papers in PubMed, 57 citations in OpenAlex.
- Oxysterol signaling in the central nervous system: cellular mechanisms and implications for neurodegeneration.Frontiers in molecular neuroscience · 2026Review
- Cut the fat: targeting cholesterol and lipid metabolism in glioblastoma.Cell death & disease · 2025Review
- Differences in gene expression between high and low tolerance rainbow trout (Oncorhynchus mykiss) to acute thermal stress.PloS one · 2025Article
- Temporal changes in mouse hippocampus transcriptome after pilocarpine-induced seizures.Frontiers in neuroscience · 2024Article
- Protective Effect of Ergothioneine against 7-Ketocholesterol-Induced Mitochondrial Damage in hCMEC/D3 Human Brain Endothelial Cells.International journal of molecular sciences · 2023Article
- Labelfree mapping and profiling of altered lipid homeostasis in the rat hippocampus after traumatic stress: Role of oxidative homeostasis.Neurobiology of stress · 2022Article
- NPC transplantation rescues sci-driven cAMP/EPAC2 alterations, leading to neuroprotection and microglial modulation.Cellular and molecular life sciences : CMLS · 2022Article
- Cholesterol as a key player in amyloid β-mediated toxicity in Alzheimer's disease.Frontiers in molecular neuroscience · 2022Review
- Alleviation of Memory Deficit by Bergenin via the Regulation of Reelin and Nrf-2/NF-κB Pathway in Transgenic Mouse Model.International journal of molecular sciences · 2021Article
- Proteomic Analysis of Mouse Brain Subjected to Spaceflight.International journal of molecular sciences · 2018Article
- Effect of Cholesterol on Membrane Fluidity and Association of Aβ Oligomers and Subsequent Neuronal Damage: A Double-Edged Sword.Frontiers in aging neuroscience · 2018Article
- Regulation of Calcium-Independent Phospholipase A2 Expression by Adrenoceptors and Sterol Regulatory Element Binding Protein-Potential Crosstalk Between Sterol and Glycerophospholipid Mediators.Molecular neurobiology · 2016Article
- Importance of Apolipoprotein A-I in Multiple Sclerosis.Frontiers in pharmacology · 2015Review
- Targeting cholesterol homeostasis to fight hearing loss: a new perspective.Frontiers in aging neuroscience · 2015Review
- Loading into nanoparticles improves quercetin's efficacy in preventing neuroinflammation induced by oxysterols.PloS one · 2014Article
- Altered fatty acid concentrations in prefrontal cortex of schizophrenic patients.Journal of psychiatric research · 2013Article
- Brain isoprenoids farnesyl pyrophosphate and geranylgeranyl pyrophosphate are increased in aged mice.Molecular neurobiology · 2012Article
- Large conductance, calcium- and voltage-gated potassium (BK) channels: regulation by cholesterol.Pharmacology & therapeutics · 2012Review
- Cholesterol loss during glutamate-mediated excitotoxicity.The EMBO journal · 2012Article
- Article
Corrections and comments
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Authors and funding
6 authors at 4 institutions in 3 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Excitotoxicity due to excess stimulation of glutamate receptors in neurons is accompanied by increased Ca(2+) influx, stimulation of Ca(2+)-dependent enzymes, ATP depletion, increase in lipid peroxidation products, and loss of glutathione. These changes resemble neurochemical alterations in acute neuronal injury (stroke, spinal cord injury, and traumatic brain injury) and chronic neurodegenerative diseases such as Alzheimer's disease. Intracerebroventricular injection of the potent glutamate analog kainate in rats results in increased cholesterol concentration in the hippocampus at short to medium time intervals, i.e., 3 days-1 week post-injection, as detected by gas chromatography-mass spectrometry in the lesioned hippocampus. This is accompanied by an early increase in levels of cholesterol biosynthetic precursors and increases in both enzymatically derived oxysterols such as 24-hydroxycholesterol and cholesterol oxidation products (COPs) generated by reactive oxygen species, including cholesterol epoxides and 7-ketocholesterol. In contrast to COPs, no change in concentration of the neurosteroid pregnenolone was found after KA injury. Cholesterol and COPs significantly increase exocytosis in cultured PC12 cells and neurons, and both oxysterols and COPs are able to induce cytotoxic and apoptotic injuries in different cell types, including neurons. Together, the findings suggest that increased cholesterol and COPs after KA excitotoxicity could themselves lead to disturbed neuronal ion homeostasis, increased neurotransmitter release, and propagation of excitotoxicity.
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