UMMS Affiliation

Department of Neurobiology

Date

8-27-2009

Document Type

Article

Subjects

Animals; Drosophila; Drosophila Proteins; Larva; Membrane Proteins; Microscopy, Confocal; Muscles; Neuroglia; Neuromuscular Junction; Presynaptic Terminals; Reverse Transcriptase Polymerase Chain Reaction; Synapses; Synaptic Transmission

Disciplines

Life Sciences | Medicine and Health Sciences | Neuroscience and Neurobiology

Abstract

Synapse remodeling is an extremely dynamic process, often regulated by neural activity. Here we show during activity-dependent synaptic growth at the Drosophila NMJ many immature synaptic boutons fail to form stable postsynaptic contacts, are selectively shed from the parent arbor, and degenerate or disappear from the neuromuscular junction (NMJ). Surprisingly, we also observe the widespread appearance of presynaptically derived "debris" during normal synaptic growth. The shedding of both immature boutons and presynaptic debris is enhanced by high-frequency stimulation of motorneurons, indicating that their formation is modulated by neural activity. Interestingly, we find that glia dynamically invade the NMJ and, working together with muscle cells, phagocytose shed presynaptic material. Suppressing engulfment activity in glia or muscle by disrupting the Draper/Ced-6 pathway results in a dramatic accumulation of presynaptic debris, and synaptic growth in turn is severely compromised. Thus actively growing NMJ arbors appear to constitutively generate an excessive number of immature boutons, eliminate those that are not stabilized through a shedding process, and normal synaptic expansion requires the continuous clearance of this material by both glia and muscle cells.

Rights and Permissions

Citation: PLoS Biol. 2009 Aug;7(8):e1000184. Epub 2009 Aug 25. Link to article on publisher's site

Comments

Co-authors Yuly F. Fuentes Medel, James A. Ashley, and Bulent Ataman are students in the Neuroscience program in the Graduate School of Biomedical Sciences (GSBS) at UMass Medical School.

Related Resources

Link to Article in PubMed

PubMed ID

19707574

 
 

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