ArticleThe Journal of physiology2015
Cholesterol modulates open probability and desensitization of NMDA receptors.
Article in The Journal of physiology, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 61 papers.
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Who cites it
61 citing papers in PubMed, 99 citations in OpenAlex.
- Mechanistic insights into PFAS-induced toxicity: from lipid membrane perturbation to ion channel and transporter dysregulation.Archives of toxicology · 2026Review
- Embryonic lead (Pb) contact impairs lipid, oxidative, and behavioral markers in zebrafish across multiple generations.Environmental research · 2026Article
- Cholesterol at the Center of Alzheimer's Disease: A Unifying Hypothesis on the Pathogenic Mechanism.Molecules (Basel, Switzerland) · 2026Review
- Caveolin-1 Attenuates Excitotoxic Signaling by Regulating NMDA, AMPA, and Kainate Receptor-Mediated Calcium Influx in Hippocampal Neuronal Cultures.International journal of molecular sciences · 2026Article
- Multiscale Cortical Remodeling Following Abrupt Visual Deafferentation in Rhegmatogenous Retinal Detachment: Imaging Transcriptomics and Neurotransmitter Mapping.CNS neuroscience & therapeutics · 2026Article
- Serum total cholesterol and low-density lipoprotein cholesterol are associated with Parkinson's disease in East Asian populations: a bidirectional Mendelian randomization study with complementary animal observation.Frontiers in aging neuroscience · 2026Article
- Cholesterol depletion inhibits BDNF-dependent spike timing-dependent plasticity at thalamo-amygdala synapses.Frontiers in cellular neuroscience · 2026Article
- Associations between plasma 24(S)-hydroxycholesterol and neuropsychological profile in fragile X syndrome.Journal of lipid research · 2025Article
- Gangliosides and Cholesterol: Dual Regulators of Neuronal Membrane Framework in Autism Spectrum Disorder.International journal of molecular sciences · 2025Review
- Regulation of NMDAR activation efficiency by environmental factors and subunit composition.The Journal of general physiology · 2025Article
- Cholesterol promotesLife science alliance · 2024Article
- Characterization of Mice Carrying a Neurodevelopmental Disease-Associated GluN2B(L825V) Variant.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2024Article
- Disease-Associated Variants in GRIN1, GRIN2A and GRIN2B genes: Insights into NMDA Receptor Structure, Function, and Pathophysiology.Physiological research · 2024Review
- Familial Alzheimer's Disease Neurons Bearing Mutations inLife (Basel, Switzerland) · 2024Article
- Nonsynonymous Mutations in Intellectual Disability and Autism Spectrum Disorder Gene PTCHD1 DisruptCells · 2024Article
- Oxysterols in Central and Peripheral Synaptic Communication.Advances in experimental medicine and biology · 2024Article
- Article
- Cholesterol- and actin-centered view of the plasma membrane: updating the Singer-Nicolson fluid mosaic model to commemorate its 50th anniversaryMolecular biology of the cell · 2023Article
- Human tau mutations in cerebral organoids induce a progressive dyshomeostasis of cholesterol.Stem cell reports · 2022Article
- Targeting NMDA Receptors at the Neurovascular Unit: Past and Future Treatments for Central Nervous System Diseases.International journal of molecular sciences · 2022Review
1 more citing papers are in PubMed but not listed here.
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Authors and funding
11 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
NMDA receptors (NMDARs) are glutamate-gated ion channels that mediate excitatory neurotransmission in the CNS. Although these receptors are in direct contact with plasma membrane, lipid-NMDAR interactions are little understood. In the present study, we aimed at characterizing the effect of cholesterol on the ionotropic glutamate receptors. Whole-cell current responses induced by fast application of NMDA in cultured rat cerebellar granule cells (CGCs) were almost abolished (reduced to 3%) and the relative degree of receptor desensitization was increased (by seven-fold) after acute cholesterol depletion by methyl-β-cyclodextrin. Both of these effects were fully reversible by cholesterol repletion. By contrast, the responses mediated by AMPA/kainate receptors were not affected by cholesterol depletion. Similar results were obtained in CGCs after chronic inhibition of cholesterol biosynthesis by simvastatin and acute enzymatic cholesterol degradation to 4-cholesten-3-one by cholesterol oxidase. Fluorescence anisotropy measurements showed that membrane fluidity increased after methyl-β-cyclodextrin pretreatment. However, no change in fluidity was observed after cholesterol enzymatic degradation, suggesting that the effect of cholesterol on NMDARs is not mediated by changes in membrane fluidity. Our data show that diminution of NMDAR responses by cholesterol depletion is the result of a reduction of the open probability, whereas the increase in receptor desensitization is the result of an increase in the rate constant of entry into the desensitized state. Surface NMDAR population, agonist affinity, single-channel conductance and open time were not altered in cholesterol-depleted CGCs. The results of our experiments show that cholesterol is a strong endogenous modulator of NMDARs.
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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.