The pathways by which neurotransmitter-filled presynaptic vesicles (SVs) are generated and recycled have been debated for a long time. Glyvuk et al (2010) in this issue of The EMBO Journal describe an unanticipated role for the clathrin adaptor AP-1 and in particular its σ1B subunit in SV recycling. SV reformation is defective in σ1B-deficient mice, which instead accumulate large endosomelike vacuoles. These defects are paired with reduced motor coordination and long-term spatial memory. This work thus not only provides novel insights into the role of clathrin/AP-1 coats in SV recycling from endosomes, but also unravels a molecular mechanism that may contribute to some forms of X-linked mental retardation.