ArticleThe Journal of neuroscience : the official journal of the Society for Neuroscience2014
Exogenous α-synuclein decreases raft partitioning of Cav2.2 channels inducing dopamine release.
Article in The Journal of neuroscience : the official journal of the Society for Neuroscience, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 45 papers.
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45 citing papers in PubMed, 65 citations in OpenAlex.
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- Mechano-bioactive hydrogel bioelectronics for mechanical-electrical-bioenergetic conversion and glia-modulating neural regeneration.Nature communications · 2025Article
- Dissociation of Clinical Outcomes and CSF Proteinopathy Biomarkers in Parkinson's Disease: Cognitive-Affective Dissociation with Specificity for Tau.Biomedicines · 2025Article
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- N-type CaNPJ Parkinson's disease · 2025Article
- The senescent synapse: A look at autophagy, calcium handling, and mitochondrial bioenergetics at the synapse in ageing and Parkinson's disease.Current research in physiology · 2025Review
- The Expression and Functionality of CBInternational journal of molecular sciences · 2024Article
- Lipid raft disruption inhibits the activation of Transient Receptor Potential Vanilloid 1, but not TRP Melastatin 3 and the voltage-gated L-type calcium channels in sensory neurons.Frontiers in cell and developmental biology · 2024Article
- Alpha-synuclein in Parkinson's disease and other synucleinopathies: from overt neurodegeneration back to early synaptic dysfunction.Cell death & disease · 2023Review
- Review
- The Role of Voltage-Gated Calcium Channels in Basal Ganglia Neurodegenerative Disorders.Current neuropharmacology · 2023Review
- Alpha-synuclein oligomers alter the spontaneous firing discharge of cultured midbrain neurons.Frontiers in cellular neuroscience · 2023Article
- Involvement of CaThe Journal of physiology · 2022Article
- α-Synuclein induced cholesterol lowering increases tonic and reduces depolarization-evoked synaptic vesicle recycling and glutamate release.NPJ Parkinson's disease · 2022Article
- Linking α-synuclein-induced synaptopathy and neural network dysfunction in early Parkinson's disease.Brain communications · 2022Review
- Alpha-synuclein increases in rodent and human spinal cord injury and promotes inflammation and tissue loss.Scientific reports · 2021Article
- Neurons and Glia Interplay in α-Synucleinopathies.International journal of molecular sciences · 2021Review
- Elucidating the Role of Lipid Rafts on G Protein-Coupled Receptor Function in the Mouse Kidney: An In Vivo Approach.Methods in molecular biology (Clifton, N.J.) · 2021Article
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Authors and funding
14 authors at 3 institutions in 4 countries.
Funding
Abstract
α-Synuclein is thought to regulate neurotransmitter release through multiple interactions with presynaptic proteins, cytoskeletal elements, ion channels, and synaptic vesicles membrane. α-Synuclein is abundant in the presynaptic compartment, and its release from neurons and glia has been described as responsible for spreading of α-synuclein-derived pathology. α-Synuclein-dependent dysregulation of neurotransmitter release might occur via its action on surface-exposed calcium channels. Here, we provide electrophysiological and biochemical evidence to show that α-synuclein, applied to rat neurons in culture or striatal slices, selectively activates Cav2.2 channels, and said activation correlates with increased neurotransmitter release. Furthermore, in vivo perfusion of α-synuclein into the striatum also leads to acute dopamine release. We further demonstrate that α-synuclein reduces the amount of plasma membrane cholesterol and alters the partitioning of Cav2.2 channels, which move from raft to cholesterol-poor areas of the plasma membrane. We provide evidence for a novel mechanism through which α-synuclein acts from the extracellular milieu to modulate neurotransmitter release and propose a unifying hypothesis for the mechanism of α-synuclein action on multiple targets: the reorganization of plasma membrane microdomains.
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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.