Summary: Learning a new motor skill reorganizes the brain’s movement circuits, and a recent study shows that astrocytes—the star-shaped glial cells long viewed as support cells—play a central, active role in that remodeling. Researchers found that astrocytes in the striatum use the phagocytic receptor MEGF10 to engulf and remove unnecessary synapses. This pruning is directed by dopamine signaling and neural activity, meaning astrocytes help translate dopamine cues into lasting structural changes that are essential for mastering new motor skills.
Key Facts
- Active pruning: Astrocytes actively remove synapses in the striatum during motor learning, refining circuits that control movement.
- MEGF10 receptor: MEGF10 on astrocytes functions as a phagocytic receptor that engulfs and eliminates weak or unnecessary synaptic contacts.
- Dopamine regulation: Dopamine helps instruct astrocytes which synapses to eliminate or preserve, with distinct effects on D1- and D2-type medium spiny neurons.
- Learning impairment: Mice lacking MEGF10 in astrocytes show poorer performance on motor-learning tasks, such as the rotarod, and disrupted signaling between motor cortex and striatum.
- Plasticity hub: Both long-term potentiation (LTP) and long-term depression (LTD) depend on astrocytic participation for proper expression during learning.
Source: Institute for Basic Science
Overview: When you learn a new motor behavior—whether a piano passage or improved balance—the brain must reconfigure the neural circuits that coordinate those movements. Traditionally, synaptic strengthening and weakening were attributed mainly to neurons. This study shifts that view by showing astrocytes are active agents in circuit refinement, not just passive support cells.
Led by Won-Suk Chung (KAIST) and Jae-Ick Kim (UNIST) with the Institute for Basic Science, the research team examined how astrocytes remodel corticostriatal synapses during motor training. They used repeated motor tasks in mice, including the rotarod test, and applied high-resolution imaging to follow individual synaptic elements as learning progressed.
The researchers observed a clear rise in astrocyte-mediated synapse elimination during motor learning. Other glial types, such as microglia and oligodendrocyte precursor cells, did not show similar changes under the same conditions, highlighting a specific role for astrocytes in sculpting motor circuits.
At the molecular level, the team identified MEGF10 (Multiple Epidermal Growth Factor-like Domains Protein 10) as a critical astrocytic phagocytic receptor required for this pruning. Selective deletion of Megf10 in astrocytes impaired both behavioral learning and electrophysiological measures: mice showed reduced motor learning, and synaptic communication between motor cortex and striatum was disrupted. Moreover, both LTP and LTD were compromised, demonstrating that astrocyte-mediated removal of synapses supports the functional plasticity needed for skill acquisition.
The investigators also probed how astrocytes decide which synapses to eliminate. They found two major regulatory signals: increased corticostriatal activity and dopamine release. Chemogenetic activation of cortical inputs or enhanced dopamine release from the substantia nigra pars compacta both amplified astrocytic synapse engulfment. Importantly, dopamine produced different structural outcomes in D1 versus D2 medium spiny neurons, and those outcomes depended on astrocytic MEGF10. In short, dopamine appears to mark or bias which connections should be strengthened, while astrocytes execute the selective pruning that consolidates the circuit.
By uncovering a dopamine- and activity-dependent mechanism by which astrocytes remodel striatal synapses, this work reframes astrocytes as essential mediators of motor learning. Because dopamine signaling is disrupted in conditions such as Parkinson’s disease and addiction, these findings may help guide future research into how circuit dysfunction arises in dopamine-related disorders and whether targeting astrocytic mechanisms could offer therapeutic avenues.
Won-Suk Chung commented, “Learning requires precise circuit rewiring that involves both forming new synapses and removing irrelevant ones. Our results identify astrocytic phagocytosis and MEGF10 as central elements of that process.”
Key Questions Answered
A: That long-held view is outdated. This study shows astrocytes act like editors: neurons form and strengthen connections, while astrocytes remove those that are unnecessary, helping to shape a coherent circuit for the learned skill.
A: Dopamine acts as a signal that highlights which pathways should be retained. Astrocytes respond to that neuromodulatory context by selectively pruning unmarked or weaker synapses, promoting a faster, more efficient circuit for the new motor behavior.
A: Potentially. Parkinson’s disease involves compromised dopamine signaling in the striatum. Understanding how dopamine and astrocytes jointly shape synaptic remodeling could point to new strategies to address movement deficits and learning dysfunction in dopamine-related disorders.
Editorial Notes
- This article was edited by a Neuroscience News editor.
- The journal paper was reviewed in full.
- Additional context was added by editorial staff.
About this neuroscience research news
Author: William Suh ([email protected])
Source: Institute for Basic Science
Contact: William Suh – Institute for Basic Science
Image: Image credited to Neuroscience News
Original Research: “Motor learning and dopamine-dependent striatal synaptic plasticity are controlled by astrocytic MEGF10” by Young-Jin Choi, Youngeun Lina Lee, Yemin Kim, Jaeseon Jeon, Jae-Ick Kim & Won-Suk Chung. Nature Communications. DOI: 10.1038/s41467-026-69129-1. Open access.
Abstract
Motor learning and dopamine-dependent striatal synaptic plasticity are controlled by astrocytic MEGF10
Dopamine regulates motor learning by modulating synaptic plasticity in striatal medium spiny neurons (MSNs). While dopamine’s role in neuronal plasticity is well established, its involvement in glia-mediated synapse remodeling has been unclear. This study demonstrates that the astrocytic phagocytic receptor MEGF10, but not MERTK, is required for eliminating corticostriatal excitatory synapses on MSNs during motor learning.
Deletion of astrocytic Megf10 impaired both long-term potentiation and long-term depression (LTP and LTD) and reduced the learning-induced increase in synaptic strength. Chemogenetic activation of corticostriatal transmission or dopamine release from the substantia nigra pars compacta selectively increased astrocytic synapse elimination. Elevated dopamine and motor learning differentially regulated postsynaptic pruning in MSNs depending on dopamine receptor subtype, producing MEGF10-dependent changes in synaptic remodeling and quantal properties. These results identify astrocytic MEGF10 as a key mediator of activity- and dopamine-dependent synapse remodeling in the striatum.