VEGF/VEGFR2 signaling regulates hippocampal axon branching during development
This study reports a novel molecular mechanism by which direct VEGF/VEGFR2 signaling on hippocampal pyramidal neurons regulates axon branching during development.
VEGF/VEGFR2 signaling falls into the category of bimodal regulators that differentially direct axonal and dendritic development in an opposite manner.
Our data provide for the first time evidence that in mammals similar processes can also modulate axon branching.
Two possibilities, non-exclusive, could explain the increased axon branching upon VEGFR2 deletion. On the one hand, the lack of VEGFR2 could lead to a decrease in the dynamics of protrusions turnover and thus increase the probability of a protrusion to become a filopodium. Our data support such a model as we observe that the absence of VEGFR2 increases the percentage of filopodia. On the other hand, a compensatory mechanism, yet unidentified, might become activated to overcome the inhibition of VEGFR2, resulting in higher branch number than in control conditions.
Common Design 