ArticleNature communications2026
Motor learning and dopamine-dependent striatal synaptic plasticity are controlled by astrocytic MEGF10.
Article in Nature communications, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. 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.
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Who cites it
2 citing papers in PubMed.
- Multi-Omics Reveals Dysregulated Neurotransmitter Systems in Aging and CNS Disorders.Aging cell · 2026Article
- SU-Eohyeol Pharmacopuncture Ameliorates Parkinson's Disease-Associated Pain via the CB1 and PPARγ Pathways in an MPTP-Induced Mouse Model.Pain research & management · 2026Article
Corrections and comments
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Authors and funding
6 authors.
Funding
Abstract
Dopamine regulates motor learning by modulating striatal synaptic plasticity in medium spiny neurons (MSNs). Despite its well-established role in synaptic plasticity, dopamine's involvement in glia-mediated synapse remodeling remains unclear. Here, we demonstrate that the astrocytic phagocytic receptor MEGF10 (Multiple Epidermal Growth Factor-like Domains Protein 10), but not MERTK (MER Proto-Oncogene, Tyrosine Kinase), is required for the elimination of corticostriatal excitatory synapses on MSNs during motor learning. Deletion of astrocytic Megf10 impaired long-term potentiation and depression (LTP and LTD), and reduced learning-induced increases in synaptic strength. Notably, chemogenetic activation of corticostriatal transmission or dopamine release from the substantia nigra pars compacta (SNc) selectively enhanced astrocytic synapse elimination. Furthermore, elevated dopamine and motor learning differentially regulated postsynaptic elimination in MSNs depending on dopamine receptor subtype, leading to MEGF10-dependent changes in synaptic remodeling and quantal properties. These findings identify astrocytic MEGF10 as a key mediator of dopamine- and activity-dependent synapse remodeling in the striatum.
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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.