ArticleJournal of lipid research2019
Cholesterol intake and statin use regulate neuronal G protein-gated inwardly rectifying potassium channels.
Article in Journal of lipid research, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 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
12 citing papers in PubMed, 24 citations in OpenAlex.
- Cholesterol-depleting dextrin depolarizes sarcolemma: the contribution of sodium / calcium channels and membrane integrity.Pflugers Archiv : European journal of physiology · 2026Article
- Medication Exposure and Risk of Dementia and Alzheimer's Disease.International journal of molecular sciences · 2024Review
- Navigating the metabolic maze: anomalies in fatty acid and cholesterol processes in Alzheimer's astrocytes.Alzheimer's research & therapy · 2024Review
- Dietary cholesterol in alcohol-associated liver disease.Immunometabolism (Cobham, Surrey) · 2023Review
- PI(4,5)PAdvances in experimental medicine and biology · 2023Article
- Cholesterol Management in Neurology: Time for Revised Strategies?Journal of personalized medicine · 2022Review
- Lipid accumulation induced by APOE4 impairs microglial surveillance of neuronal-network activity.Cell stem cell · 2022Article
- Neuronal G protein-gated KAmerican journal of physiology. Cell physiology · 2022Review
- Statins and cognition: Modifying factors and possible underlying mechanisms.Frontiers in aging neuroscience · 2022Review
- Advances in stimulated Raman scattering imaging for tissues and animals.Quantitative imaging in medicine and surgery · 2021Review
- Mammalian cell and tissue imaging using Raman and coherent Raman microscopy.Wiley interdisciplinary reviews. Systems biology and medicine · 2020Review
- Ion Channels of the Islets in Type 2 Diabetes.Journal of molecular biology · 2020Review
Corrections and comments
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Authors and funding
3 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Cholesterol, a critical component of the cellular plasma membrane, is essential for normal neuronal function. Cholesterol content is highest in the brain, where most cholesterol is synthesized de novo; HMG-CoA reductase controls the synthesis rate. Despite strict control, elevated blood cholesterol levels are common and are associated with various neurological disorders. G protein-gated inwardly rectifying potassium (GIRK) channels mediate the actions of inhibitory brain neurotransmitters. Loss of GIRK function enhances neuron excitability; gain of function reduces neuronal activity. However, the effect of dietary cholesterol or HMG-CoA reductase inhibition (i.e., statin therapy) on GIRK function remains unknown. Using a rat model, we compared the effects of a high-cholesterol versus normal diet both with and without atorvastatin, a widely prescribed HMG-CoA reductase inhibitor, on neuronal GIRK currents. The high-cholesterol diet increased hippocampal CA1 region cholesterol levels and correspondingly increased neuronal GIRK currents. Both phenomena were reversed by cholesterol depletion in vitro. Atorvastatin countered the high-cholesterol diet effects on neuronal cholesterol content and GIRK currents; these effects were reversed by cholesterol enrichment in vitro. Our findings suggest that high-cholesterol diet and atorvastatin therapy affect ion channel function in the brain by modulating neuronal cholesterol levels.
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