Synaptic membrane rafts: traffic lights for local neurotrophin signaling?
Open accessAbstract
Lipid rafts, cholesterol and lipid rich microdomains, are believed to play important roles as platforms for the partitioning of transmembrane and synaptic proteins involved in synaptic signaling, plasticity, and maintenance. There is increasing evidence of a physical interaction between post-synaptic densities and post-synaptic lipid rafts. Localization of proteins within lipid rafts is highly regulated, and therefore lipid rafts may function as traffic lights modulating and fine-tuning neuronal signaling. The tyrosine kinase neurotrophin receptors (Trk) and the low-affinity p75 neurotrophin receptor (p75(NTR)) are enriched in neuronal lipid rafts together with the intermediates of downstream signaling pathways, suggesting a possible role of rafts in neurotrophin signaling. Moreover, neurotrophins and their receptors are involved in the regulation of cholesterol metabolism. Cholesterol is an important component of lipid rafts and its depletion leads to gradual loss of synapses, underscoring the importance of lipid rafts for proper neuronal function. Here, we review and discuss the idea that translocation of neurotrophin receptors in synaptic rafts may account for the selectivity of their transduced signals.
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Several signaling pathways disrupted in RTT, including BDNF/TrkB signaling, glutamatergic neurotransmission and activity-dependent synaptic plasticity, depend on the integrity of lipid rafts.
“and several signaling pathways that are disrupted in RTT, including BDNF/TrkB signaling, glutamatergic neurotransmission and activity-dependent synaptic plasticity, are known to depend on the integrity of lipid rafts for their proper organization and function (Sebastião et al., 2013;Zonta & Minichiello, 2013).”
From Impaired astrocyte-to-neuron cholesterol trafficking drives synaptic dysfunction in Rett syndrome (2026) · cites this paper as Zonta & Minichiello, 2013
The section “Lipid raft regulation of BDNF signaling at synapses” reports that disrupting rafts abolished BDNF’s effects on synaptic transmission and plasticity, and discusses raft-associated glutamate receptors. It does not establish that these pathways are disrupted in RTT, and it explicitly says lipid rafts are not required for BDNF/TrkB signaling involved in neuronal survival. Thus the claim’s unqualified dependence on raft integrity is broader than the review supports. (LLM, conf=0.86)
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- Authors
- Zonta, B., & Minichiello, L.
- Affiliations
- University of Oxford (GB)
- Corresponding author
- Minichiello, Liliana
- ORCID
- Minichiello, Liliana
- Venue
- Frontiers in Synaptic Neuroscience
- Publisher
- Frontiers Media SA
- Published
- 2013
- Volume
- 5
- Pages
- 9-9
- ISSN
- 1663-3563 (ISSN-L)
- PMC
- PMC3798807
- OpenAlex
- W2169251909
- Cited by
- 41
- References
- 57
- Citations by year
- 2026: 2 · 2025: 1 · 2024: 3 · 2023: 3 · 2022: 3 · 2021: 3 · 2020: 3 · 2019: 3 · 2018: 1 · 2017: 6 · 2016: 4 · 2015: 6 · 2014: 3
- FWCI
- 0.44
- Type
- journal article
- Language
- en
- Open access
- gold
- doi.org
- Licence
- cc-by
- Locations
- Frontiers in Synaptic Neuroscience (publishedVersion, cc-by)
- Europe PMC (PubMed Central) (publishedVersion, cc-by)
- PubMed Central (publishedVersion, cc-by)
- PubMed (publishedVersion)
- DOAJ (DOAJ: Directory of Open Access Journals) (submittedVersion, cc-by-sa)
- Edinburgh Research Explorer (University of Edinburgh) (submittedVersion, cc-by)
- Topics
- Life Sciences › Neuroscience › Cellular and Molecular Neuroscience › Nerve injury and regeneration
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Lipid Membrane Structure and Behavior
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Cell Biology › Caveolin-1 and cellular processes
- Keywords
- lipid rafts, neurotrophin signaling, Trk receptors, p75 neurotrophin receptor, cholesterol, postsynaptic density, synaptic plasticity, receptor translocation, signal transduction, synapse maintenance
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.
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