Multiple mechanisms mediate cholesterol-induced synaptogenesis in a CNS neuron
Abstract
Neurons undergo a complex differentiation process that endows them with the ability to generate electrical signals and to transmit them via synaptic connections. There is increasing evidence that glial cells regulate specific aspects of neuronal differentiation including synapse formation, but the underlying mechanisms are not well understood. Here, we show how glia-derived cholesterol promotes the development of synapses in microcultures of highly purified retinal ganglion cells (RGCs) from postnatal rats. We identify dendrite differentiation as rate limiting step for glia-induced synaptogenesis and we show that this process requires cholesterol. Furthermore, we show that cholesterol enhances directly presynaptic differentiation and that it is essential for continuous synaptogenesis and for the stability of evoked transmitter release. These results reveal new roles of cholesterol in neuronal differentiation and underline the importance of neuron-glia interactions during brain development.
Integrity signals
Registry
Cites
Statistics
Claims the paper makes
Claims other papers make about this one
Each is checked against this paper’s own text: does it say what the citing paper says it does?
Cholesterol is essential for maintaining synaptic activity.
“removal of cholesterol diminished the size of evoked excitatory postsynaptic currents, suggesting that cholesterol is essential for maintaining synaptic activity [48].”
From MicroRNAs in brain cholesterol metabolism and their implications for Alzheimer's disease (2016) · cites this paper as [48]
Astrocytes are the main source of cholesterol in the brain.
“Astrocytes are the main source of cholesterol in the brain, and cholesterol secreted by astrocytes has a role in synaptic formation and maintenance (Goritz et al., 2005;J.-P. Liu et al., 2010;Pfrieger, 2003).”
From Impaired astrocyte-to-neuron cholesterol trafficking drives synaptic dysfunction in Rett syndrome (2026) · cites this paper as Goritz et al., 2005
Cholesterol secreted by astrocytes has a role in synaptic formation and maintenance.
“Astrocytes are the main source of cholesterol in the brain, and cholesterol secreted by astrocytes has a role in synaptic formation and maintenance (Goritz et al., 2005;J.-P. Liu et al., 2010;Pfrieger, 2003).”
From Impaired astrocyte-to-neuron cholesterol trafficking drives synaptic dysfunction in Rett syndrome (2026) · cites this paper as Goritz et al., 2005
Cholesterol depletion is associated with dendritic spine loss and synaptic degeneration, whereas cholesterol supplementation promotes synapse formation and enhances synaptic activity.
“Indeed cholesterol depletion has been associated with dendritic spine loss and synaptic degeneration, whereas its supplementation promotes synapse formation and enhances synaptic activity (Goritz et al., 2005;Liu et al., 2010;Mauch et al., 2001).”
From Impaired astrocyte-to-neuron cholesterol trafficking drives synaptic dysfunction in Rett syndrome (2026) · cites this paper as Goritz et al., 2005
Cholesterol has a well-established role in synaptic development and maintenance.
“This choice was driven by the well-established role of cholesterol in synaptic development and maintenance (Goritz et al., 2005;J.-P. Liu et al., 2010;Pfrieger, 2003)”
From Impaired astrocyte-to-neuron cholesterol trafficking drives synaptic dysfunction in Rett syndrome (2026) · cites this paper as Goritz et al., 2005
The citation lists haven’t been fetched yet
References 65 · Cited by 330
- Authors
- Goritz, C., Mauch, D. H., & Pfrieger, F. W.
- Affiliations
- Centre National de la Recherche Scientifique (FR)
- Corresponding author
- Pfrieger, Frank W.
- ORCID
- Pfrieger, Frank W.
- Venue
- Molecular and Cellular Neuroscience
- Publisher
- Elsevier BV
- Published
- 2005-06
- Volume
- 29
- Issue
- 2
- Pages
- 190-201
- ISSN
- 1044-7431 (ISSN-L)
- OpenAlex
- W2025872849
- Cited by
- 330
- References
- 65
- Citations by year
- 2026: 8 · 2025: 15 · 2024: 22 · 2023: 31 · 2022: 21 · 2021: 23 · 2020: 28 · 2019: 22 · 2018: 9 · 2017: 5 · 2016: 9 · 2015: 13 · 2014: 16 · 2013: 10 · 2012: 15
- FWCI
- 4.94
- Type
- journal article
- Language
- en
- Open access
- closed
- Locations
- Molecular and Cellular Neuroscience (publishedVersion)
- PubMed (publishedVersion)
- HAL (submittedVersion)
- Funders
- Deutsche Forschungsgemeinschaft
- Centre National de la Recherche Scientifique
- Topics
- Life Sciences › Neuroscience › Cellular and Molecular Neuroscience › Neuroscience and Neuropharmacology Research
- Life Sciences › Neuroscience › Neurology › Neuroinflammation and Neurodegeneration Mechanisms
- Life Sciences › Neuroscience › Developmental Neuroscience › Neurogenesis and neuroplasticity mechanisms
- Keywords
- cholesterol, synaptogenesis, retinal ganglion cells, neuron-glia interactions, presynaptic differentiation, neurotransmitter release, neuronal differentiation, retinal development
- MeSH terms
- Animals, Animals, Newborn, Cell Communication, Cell Differentiation, Cells, Cultured, Central Nervous System, Cholesterol, Electric Stimulation, Synaptic Transmission, Neuroglia, Retinal Ganglion Cells, Synapses, Synapsins, Culture Media, Conditioned, Receptors, AMPA, Neurotransmitter Agents, Patch-Clamp Techniques, Excitatory Postsynaptic Potentials, Rats
About these checks
Registry, retraction, Cites and statistics results are computed, not judged, with one exception: a printed reference that no index lists is read once by a model before it counts as a citation error. Claims are extracted by a model and kept only when their quote appears verbatim in the text; each cited source is then checked, with a model’s help, for whether it says what the claim relies on. Those verdicts can be wrong — read the claim’s quote and the cited source before relying on one.
Statistics and arithmetic are recomputed, not judged.
Confidence bands are shown only for fields calibrated on our annotated test set. None is calibrated yet, so no band is shown.
What counts as a claim ›How we measure confidence ›How we check this ›
Are you an author, or do you see a problem with this page? Request a review