title: Glutamate regulates actin-based motility in axonal filopodia.
abstract: The dynamics of axonal arbors during synaptogenesis and their plasticity in the adult nervous system remain poorly understood. Axonal filopodia, which emerge from the shaft of axonal branches and contain small synaptic vesicle clusters, initiate synaptic formation. We found that the movement of axonal filopodia is strongly inhibited by the neurotransmitter glutamate. This inhibitory effect is local, requires extracellular Ca2+, and can be blocked by CNQX treatment but not by NMDA, implicating axonal AMPA/kainate glutamate receptors. Transport and exo-endocytic recycling of synaptic vesicle packages in filopodia are not affected. These results reveal that the effect of glutamate on axonal filopodia is similar to its previously described effect on dendritic spines. Our results raise the possibility that axonal ionotropic glutamate receptors are also involved in synaptic plasticity in the adult nervous system.
authors.affiliation: Howard Hughes Medical Institute and Department of Cell Biology, Boyer Center for Molecular Medicine, Yale University School of Medicine, 295 Congress Avenue, PO Box 9812, New Haven, Connecticut 06515, USA.
authors.forename: S
authors.initials: S
authors.lastname: Chang
authors.forename: P
authors.initials: P
authors.lastname: De Camilli
mesh_terms: D000199:Actins / Q000037:antagonists & inhibitors / Q000235:genetics / Q000378:metabolism*; D000818:Animals; D019086:Bridged Bicyclo Compounds, Heterocyclic / Q000494:pharmacology; D002118:Calcium / Q000378:metabolism; D015220:Calcium Channels / Q000187:drug effects / Q000378:metabolism; D002454:Cell Differentiation / Q000187:drug effects / Q000502:physiology*; D002465:Cell Movement / Q000187:drug effects / Q000502:physiology*; D002478:Cells, Cultured / Q000166:cytology / Q000187:drug effects / Q000378:metabolism; D002490:Central Nervous System / Q000166:cytology / Q000196:embryology* / Q000378:metabolism; D018698:Glutamic Acid / Q000187:drug effects / Q000378:metabolism*; D049452:Green Fluorescent Proteins; D020439:Growth Cones / Q000187:drug effects / Q000378:metabolism* / Q000648:ultrastructure; D006624:Hippocampus / Q000166:cytology / Q000187:drug effects / Q000378:metabolism; D007150:Immunohistochemistry; D008164:Luminescent Proteins / Q000235:genetics; D009473:Neuronal Plasticity / Q000187:drug effects / Q000235:genetics; D011554:Pseudopodia / Q000187:drug effects / Q000378:metabolism* / Q000648:ultrastructure; D051381:Rats; D018091:Receptors, AMPA / Q000819:agonists / Q000037:antagonists & inhibitors / Q000378:metabolism; D016194:Receptors, N-Methyl-D-Aspartate / Q000819:agonists / Q000037:antagonists & inhibitors / Q000378:metabolism; D013844:Thiazoles / Q000494:pharmacology; D053778:Thiazolidines; D016875:tau Proteins / Q000378:metabolism
chemical_list: D000199:Actins; D019086:Bridged Bicyclo Compounds, Heterocyclic; D015220:Calcium Channels; D008164:Luminescent Proteins; D018091:Receptors, AMPA; D016194:Receptors, N-Methyl-D-Aspartate; D013844:Thiazoles; D053778:Thiazolidines; D016875:tau Proteins; D049452:Green Fluorescent Proteins; D018698:Glutamic Acid; C037067:latrunculin A; D002118:Calcium