1. Friedrich-Miescher-Laboratorium der Max-Planck-Gesellschaft, Spemannstrasse 37-39, 72076 Tübingen, Germany
2. Department of Biology, McGill University , 1205 Avenue Docteur Penfield, Montréal , Québec H3A 1B1, Canada

Correspondence to: Christoph M. Schuster¹ Correspondence and requests for material should be addressed to C.M.S. (e-mail: Email: Christoph.Schuster@tuebingen.mpg.de).

Long-term synaptic plasticity may be associated with structural rearrangements within the neuronal circuitry^{1, 2}. Although the molecular mechanisms governing such activity-controlled morphological alterations are mostly elusive, polysomal accumulations at the base of developing dendritic spines³ and the activity-induced synthesis of synaptic components suggest that localized translation is involved during synaptic plasticity^{4, 5}. Here we show that large aggregates of translational components as well as messenger RNA of the postsynaptic glutamate receptor subunit DGluR-IIA⁶ are localized within subsynaptic compartments of larval neuromuscular junctions of Drosophila melanogaster. Genetic models of junctional plasticity⁷ and genetic manipulations using the translation initiation factors eIF4E⁸ and poly(A)-binding protein⁹ showed an increased occurrence of subsynaptic translation aggregates. This was associated with a significant increase in the postsynaptic DGluR-IIA protein levels and a reduction in the junctional expression of the cell-adhesion molecule Fasciclin II. In addition, the efficacy of junctional neurotransmission and the size of larval neuromuscular junctions were significantly increased. Our results therefore provide evidence for a postsynaptic translational control of long-term junctional plasticity.