The paper presents neuronal NMDARs as regulators of zebrafish brain vascular development through neurovascular communication.
First-pass extracted concept
neuronal NMDA receptors
Aliases
NMDARs, N-methyl-D-aspartate receptors
Extracted Explainers
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Linked Claims
The vascular defects caused by neuronal NMDA receptor dysfunction are attributed to reduced growth of vascular endothelial tip cells at the leading edge of brain angiogenic sprouts.
These defects are attributed to the reduced growth of vascular endothelial tip cells (ETCs) situating at the leading edge of brain angiogenic sprouts.
Dysfunction of neuronal NMDA receptors impairs formation of the zebrafish brain vasculature and abolishes neural activity-induced enhancement of brain vascular development.
Dysfunction of neuronal NMDARs impairs the formation of the zebrafish brain vasculature and abrogates the neural activity-induced enhancement of the brain vascular development.
Neuronal NMDA receptors regulate zebrafish brain vascular development via neurovascular communication.
Here, we report that NMDARs expressed on neurons regulate brain vascular development via neurovascular communication.
Neuronal NMDA receptor dysfunction down-regulates neuronal vascular endothelial growth factor expression and subsequent endothelial tip-cell calcium activity, impairing endothelial tip-cell growth.
At the molecular level, NMDAR dysfunction down-regulates neuronal expression of vascular endothelial growth factor and subsequent global Ca2+ activities of ETCs, thereby impairing ETC growth.