Researchers identified MEGF10, a phagocytic receptor on astrocytes, as essential for eliminating corticostriatal synapses during motor skill acquisition. When MEGF10 was deleted from astrocytes, mice showed impaired long-term potentiation and depression, plus reduced learning-induced synaptic strengthening in medium spiny neurons. Dopamine release from the substantia nigra specifically enhanced astrocytic synapse elimination through MEGF10-dependent pathways. This discovery fundamentally shifts our understanding of how motor learning occurs at the cellular level. Traditional models focused on strengthening synapses, but this work reveals that selective synapse elimination by astrocytes is equally critical for acquiring new motor skills. The finding bridges two major research areas: dopamine's role in motor learning and glial cells' active participation in synaptic remodeling. For neurological conditions involving motor dysfunction like Parkinson's disease, this suggests therapeutic targets beyond just dopamine replacement. The astrocytic elimination process appears highly regulated, responding differentially to dopamine receptor subtypes and activity patterns. This precision argues against viewing synapse loss as merely destructive, instead positioning it as a sophisticated neural editing mechanism essential for optimal motor performance and learning efficiency.