Abstract
BackgroundRetinotectal map formation develops via topographically specific guidance and branching of retinal axons in their target area. This process is controlled, in part, by reverse signalling of ephrinAs expressed on retinal axons. As glycosylphosphatidylinositol-anchored molecules, ephrinAs require transmembrane co-receptors to exert this function, for which the two neurotrophin receptors, p75NTR and TrkB, were recently proposed.ResultsWe show here that the ligands for these receptors, the brain-derived neurotrophic factor precursor (proBDNF) and its processed form, BDNF, respectively, control the branching of retinal axons antagonistically, which they mediate by inducing the corresponding neurotrophin receptor-ephrinA complexes. Moreover, scavenging proneurotrophins, by adding antibodies specific for the pro-domain of proBNDF or a soluble extracellular domain of p75NTR, abolish repellent ephrinA reverse signalling in the stripe assay.ConclusionsThis indicates that retinal cells secrete proneurotrophins, inducing the ephrinA-p75NTR interaction and enabling repellent axon guidance. The antagonistic functions of proBDNF and BDNF raise the possibility that topographic branching is controlled by local control of processing of proneurotrophins.
Highlights
Retinotectal map formation develops via topographically specific guidance and branching of retinal axons in their target area
This study investigates whether the interaction of ephrinAs with either TrkB or p75NTR results in antagonistic effects on axon guidance and branching of retinal axons [22]
Ligand-promoted interaction of ephrinA5 with p75NTR We have recently shown that the interaction between ephrinAs and TrkB is promoted by the ligand brain derived neurotrophic factor (BDNF) [6]
Summary
Retinotectal map formation develops via topographically specific guidance and branching of retinal axons in their target area. This process is controlled, in part, by reverse signalling of ephrinAs expressed on retinal axons. The retino-tectal projection is a well suited model system to investigate the formation of topographic maps and the control of local axon branching In this projection, retinal ganglion cell (RGC) axons grow into the tectum in a non-topographic manner and initially overshoot their future termination zones. The final map is a product of both activity-independent and activity-dependent processes [1,2,3] Some aspects of this mapping process are controlled by retinally expressed ephrinA molecules, with higher expression on nasal than on temporal retinal axons. This differential expression mediates a repulsion of nasal axons from parts of the target area expressing
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