ArticleScience advances2026
α-Synuclein expression is required for somatodendritic dopamine release and immediate early gene induction.
Article in Science advances, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 2 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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
2 citing papers in PubMed.
- Rebalancing α-Synuclein Clearance: Novel Therapeutic Frontiers in Parkinson's Disease.Neuromolecular medicine · 2026Review
- α-Synuclein pathology differentially alters T-type calcium currents in vulnerable and resilient substantia nigra dopaminergic subpopulations.bioRxiv : the preprint server for biology · 2026Article
Corrections and comments
- Erratum issued
Authors and funding
12 authors.
Funding
Abstract
α-Synuclein (αSyn) is a presynaptic protein of unestablished physiological function that plays a central role in Parkinson's disease neuropathology. To date, the reported effects of αSyn expression on the kinetics of axonal synaptic vesicle exocytosis and membrane cycling have been relatively small. In contrast, we report that αSyn is the major modulator of substantia nigra somatodendritic dopamine release, a little-understood form of neurotransmission that is central to sensorimotor and basal ganglia circuitry. This regulation is due to a previously unknown role for αSyn in controlling the activity of the L-type calcium ion channels (LTCC), which are also implicated in Parkinson's pathogenesis. αSyn-deficient neurons further display decreased spike frequency adaptation, hippocampal LTCC-dependent long-term potentiation, and immediate early gene induction, functions that are essential for synaptic adaptation and neuronal plasticity.
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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 Socratic graph.