English
 
Help Privacy Policy Disclaimer
  Advanced SearchBrowse

Item

ITEM ACTIONSEXPORT

Released

Journal Article

EphrinB2 regulates VEGFR2 during dendritogenesis and hippocampal circuitry development

MPS-Authors
/persons/resource/persons38744

Acker-Palmer,  Amparo
Neurovascular interface Group, Max Planck Institute for Brain Research, Max Planck Society;

External Resource
Fulltext (public)
There are no public fulltexts stored in PuRe
Supplementary Material (public)
There is no public supplementary material available
Citation

Harde, E., Nicholson, L., Furones Cuadrado, B., Bissen, D., Wigge, S., Urban, S., et al. (2019). EphrinB2 regulates VEGFR2 during dendritogenesis and hippocampal circuitry development. Elife, 8. doi:10.7554/eLife.49819.


Cite as: http://hdl.handle.net/21.11116/0000-0008-0C1E-B
Abstract
Vascular endothelial growth factor (VEGF) is an angiogenic factor that play important roles in the nervous system, although it is still unclear which receptors transduce those signals in neurons. Here, we show that in the developing hippocampus VEGFR2 (also known as KDR or FLK1) is expressed specifically in the CA3 region and it is required for dendritic arborization and spine morphogenesis in hippocampal neurons. Mice lacking VEGFR2 in neurons (Nes-cre Kdr(lox/-)) show decreased dendritic arbors and spines as well as a reduction in long-term potentiation (LTP) at the associational-commissural - CA3 synapses. Mechanistically, VEGFR2 internalization is required for VEGF-induced spine maturation. In analogy to endothelial cells, ephrinB2 controls VEGFR2 internalization in neurons. VEGFR2-ephrinB2 compound mice (Nes-cre Kdr(lox/+) Efnb2(lox/+)) show reduced dendritic branching, reduced spine head size and impaired LTP. Our results demonstrate the functional crosstalk of VEGFR2 and ephrinB2 in vivo to control dendritic arborization, spine morphogenesis and hippocampal circuitry development.