ArticleJournal of neurophysiology2012
Regulation of presynaptic strength by controlling Ca2+ channel mobility: effects of cholesterol depletion on release at the cone ribbon synapse.
Article in Journal of neurophysiology, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 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.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
19 citing papers in PubMed, 32 citations in OpenAlex.
- Astrocytic Cholesterol Fine-Tunes the Balance of Different Modes of Synaptic Exo- and Endocytosis.bioRxiv : the preprint server for biology · 2026Article
- Cholesterol imbalance and neurotransmission defects in neurodegeneration.Experimental & molecular medicine · 2024Review
- Bottlenecks in the Investigation of Retinal Sterol Homeostasis.Biomolecules · 2024Review
- Oxysterols in Central and Peripheral Synaptic Communication.Advances in experimental medicine and biology · 2024Article
- Article
- Requirement of Cholesterol for Calcium-Dependent Vesicle Fusion by Strengthening Synaptotagmin-1-Induced Membrane Bending.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2023Article
- Mechanisms controlling the trafficking, localization, and abundance of presynaptic CaFrontiers in molecular neuroscience · 2022Review
- Transmission at rod and cone ribbon synapses in the retina.Pflugers Archiv : European journal of physiology · 2021Review
- Voltage-Gated Calcium Channels: Key Players in Sensory Coding in the Retina and the Inner Ear.Physiological reviews · 2018Review
- Endocytosis sustains release at photoreceptor ribbon synapses by restoring fusion competence.The Journal of general physiology · 2018Article
- Promotion of endocytosis efficiency through an ATP-independent mechanism at rat calyx of Held terminals.The Journal of physiology · 2017Article
- Cyclodextrins and Iatrogenic Hearing Loss: New Drugs with Significant Risk.Frontiers in cellular neuroscience · 2017Review
- Fluid flow facilitates inward rectifier KScientific reports · 2016Article
- Cholesterol regulates multiple forms of vesicle endocytosis at a mammalian central synapse.Journal of neurochemistry · 2015Article
- LTP-triggered cholesterol redistribution activates Cdc42 and drives AMPA receptor synaptic delivery.The Journal of cell biology · 2015Article
- 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
- Lateral mobility of L-type calcium channels in synaptic terminals of retinal bipolar cells.Molecular vision · 2013Article
- Tracking quantum dot-tagged calcium channels at vertebrate photoreceptor synapses: retinal slices and dissociated cells.Current protocols in neuroscience · 2013Article
- Rapid synaptic vesicle endocytosis in cone photoreceptors of salamander retina.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2012Article
Corrections and comments
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Authors and funding
5 authors at 2 institutions in 1 country.
Funding
Abstract
Synaptic communication requires proper coupling between voltage-gated Ca(2+) (Ca(V)) channels and synaptic vesicles. In photoreceptors, L-type Ca(V) channels are clustered close to synaptic ribbon release sites. Although clustered, Ca(V) channels move continuously within a confined domain slightly larger than the base of the ribbon. We hypothesized that expanding Ca(V) channel confinement domains should increase the number of channel openings needed to trigger vesicle release. Using single-particle tracking techniques, we measured the expansion of Ca(V) channel confinement domains caused by depletion of membrane cholesterol with cholesterol oxidase or methyl-β-cyclodextrin. With paired whole cell recordings from cones and horizontal cells, we then determined the number of Ca(V) channel openings contributing to cone Ca(V) currents (I(Ca)) and the number of vesicle fusion events contributing to horizontal cell excitatory postsynaptic currents (EPSCs) following cholesterol depletion. Expansion of Ca(V) channel confinement domains reduced the peak efficiency of release, decreasing the number of vesicle fusion events accompanying opening of each Ca(V) channel. Cholesterol depletion also inhibited exocytotic capacitance increases evoked by brief depolarizing steps. Changes in efficiency were not due to changes in I(Ca) amplitude or glutamate receptor properties. Replenishing cholesterol restored Ca(V) channel domain size and release efficiency to control levels. These results indicate that cholesterol is important for organizing the cone active zone. Furthermore, the finding that cholesterol depletion impairs coupling between channel opening and vesicle release by allowing Ca(V) channels to move further from release sites shows that changes in presynaptic Ca(V) channel mobility can be a mechanism for adjusting synaptic strength.
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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.