ArticleBiophysical journal2005
Caveolin-1 expression and membrane cholesterol content modulate N-type calcium channel activity in NG108-15 cells.
Article in Biophysical journal, 2005. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 46 papers.
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Who cites it
46 citing papers in PubMed.
- Cholesterol-binding motifs in STING that control endoplasmic reticulum retention mediate anti-tumoral activity of cholesterol-lowering compounds.Nature communications · 2024Article
- Direct modulation of G protein-gated inwardly rectifying potassium (GIRK) channels.Frontiers in physiology · 2024Review
- Are There Lipid Membrane-Domain Subtypes in Neurons with Different Roles in Calcium Signaling?Molecules (Basel, Switzerland) · 2023Review
- CaAdvances in experimental medicine and biology · 2023Article
- A molecular switch controls the impact of cholesterol on a Kir channel.Proceedings of the National Academy of Sciences of the United States of America · 2022Article
- Mechanotransduction in hippocampal neurons operates under localized low picoNewton forces.iScience · 2022Article
- Endocytosis of Connexin 36 is Mediated by Interaction with Caveolin-1.International journal of molecular sciences · 2020Article
- Cholesterol intake and statin use regulate neuronal G protein-gated inwardly rectifying potassium channels.Journal of lipid research · 2019Article
- Reduced membrane cholesterol limits pulmonary endothelial CaAmerican journal of physiology. Heart and circulatory physiology · 2017Article
- Cholesterol up-regulates neuronal G protein-gated inwardly rectifying potassium (GIRK) channel activity in the hippocampus.The Journal of biological chemistry · 2017Article
- Loss of parkin promotes lipid rafts-dependent endocytosis through accumulating caveolin-1: implications for Parkinson's disease.Molecular neurodegeneration · 2015Article
- Isoform dependent regulation of human HCN channels by cholesterol.Scientific reports · 2015Article
- Inhibition of CaV2.3 channels by NK1 receptors is sensitive to membrane cholesterol but insensitive to caveolin-1.Pflugers Archiv : European journal of physiology · 2015Article
- Cholesterol removal from adult skeletal muscle impairs excitation-contraction coupling and aging reduces caveolin-3 and alters the expression of other triadic proteins.Frontiers in physiology · 2015Article
- Raft-partitioning of calcium channels regulates their function.Channels (Austin, Tex.) · 2015Article
- Identification of a cholesterol-binding pocket in inward rectifier K(+) (Kir) channels.Biophysical journal · 2014Article
- Exogenous α-synuclein decreases raft partitioning of Cav2.2 channels inducing dopamine release.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2014Article
- Poly(ethylene glycol)-cholesterol inhibits L-type Ca2+ channel currents and augments voltage-dependent inactivation in A7r5 cells.PloS one · 2014Article
- Increasing Membrane Cholesterol Level Increases the Amyloidogenic Peptide by Enhancing the Expression of Phospholipase C.Journal of neurodegenerative diseases · 2013Article
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5 authors.
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Abstract
Caveolins are the main structural proteins of glycolipid/cholesterol-rich plasmalemmal invaginations, termed caveolae. In addition, caveolin-1 isoform takes part in membrane remodelling as it binds and transports newly synthesized cholesterol from endoplasmic reticulum to the plasma membrane. Caveolin-1 is expressed in many cell types, including hippocampal neurons, where an abundant SNAP25-caveolin-1 complex is detected after induction of persistent synaptic potentiation. To ascertain whether caveolin-1 influences neuronal voltage-gated Ca2+ channel basal activity, we stably expressed caveolin-1 into transfected neuroblastoma x glioma NG108-15 hybrid cells [cav1(+) clone] that lack endogenous caveolins but express N-type Ca2+ channels upon cAMP-induced neuronal differentiation. Whole-cell patch-clamp recordings of cav1(+) cells demonstrated that N-type current density was reduced in size by approximately 70% without any significant change in the time course of activation and inactivation and voltage dependence. Moreover, the cav1(+) clone exhibited a significantly increased proportion of membrane cholesterol compared to wild-type NG108-15 cells. To gain insight into the mechanism underlying caveolin-1 lowering of N-current density, and more precisely to test whether this was indirectly caused by caveolin-1-induced enhancement of membrane cholesterol, we compared single N-type channel activities in cav1(+) clone and wild-type NG108-15 cells enriched with cholesterol after exposure to a methyl-beta-cyclodextrin-cholesterol complex. A lower Ca2+ channel activity was recorded from cell-attached patches of both cell types, thus supporting the view that the increased proportion of membrane cholesterol is ultimately responsible for the effect. This is due to a reduction in the probability of channel opening caused by a significant decrease of channel mean open time and by an increase of the frequency of null sweeps.
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