6533b85dfe1ef96bd12bea91
RESEARCH PRODUCT
Clustering transmembrane-agrin induces filopodia-like processes on axons and dendrites
Godela BittcherMaik AnniesJürgen LöschingerElmar PortenStefan WöllRene RamsegerStephan KrögerChristian AbrahamMarkus A. Rüeggsubject
animal structuresDendritic spineTime FactorsNeuriteCytochalasin BGrowth ConesVideo microscopyChick EmbryoBiologyNervous SystemAntibodiesCellular and Molecular NeuroscienceMicemedicineNeuritesAnimalsAgrinPseudopodiaGrowth coneCytoskeletonMolecular BiologyCells CulturedCytoskeletonAgrinMicroscopy VideoDose-Response Relationship DrugCell MembraneCell DifferentiationCell BiologyDendritesCell biologymedicine.anatomical_structurenervous systemAnimals NewbornNeuronFilopodiadescription
The transmembrane form of agrin (TM-agrin) is primarily expressed in the CNS, particularly on neurites. To analyze its function, we clustered TM-agrin on neurons using anti-agrin antibodies. On axons from the chick CNS and PNS as well as on axons and dendrites from mouse hippocampal neurons anti-agrin antibodies induced the dose- and time-dependent formation of numerous filopodia-like processes. The processes appeared within minutes after antibody addition and contained a complex cytoskeleton. Formation of processes required calcium, could be inhibited by cytochalasine D, but was not influenced by staurosporine, heparin or pervanadate. Time-lapse video microscopy revealed that the processes were dynamic and extended laterally along the entire length of the neuron. The lateral processes had growth cones at their tips that initially adhered to the substrate, but subsequently collapsed and were retracted. These data provide the first evidence for a specific role of TM-agrin in shaping the cytoskeleton of neurites in the developing nervous system.
| year | journal | country | edition | language |
|---|---|---|---|---|
| 2005-09-22 |