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Activation of NMDA receptors in brain endothelial cells increases transcellular permeabilityopen access

Authors
Kim, Kyu-SungJeon, Min TaeKim, Eun SeonLee, Chan HeeKim, Do-Geun
Issue Date
Sep-2022
Publisher
BioMed Central
Citation
Fluids and Barriers of the CNS, v.19, no.1
Journal Title
Fluids and Barriers of the CNS
Volume
19
Number
1
URI
http://scholarworks.bwise.kr/kbri/handle/2023.sw.kbri/203
DOI
10.1186/s12987-022-00364-6
ISSN
2045-8118
Abstract
Neurovascular coupling is a precise mechanism that induces increased blood flow to activated brain regions, thereby providing oxygen and glucose. In this study, we hypothesized that N-methyl-D-aspartate (NMDA) receptor signaling, the most well characterized neurotransmitter signaling system which regulates delivery of essential molecules through the blood-brain barrier (BBB). Upon application of NMDA in both in vitro and in vivo models, increased delivery of bioactive molecules that was mediated through modulation of molecules involved in molecular delivery, including clathrin and caveolin were observed. Also, NMDA activation induced structural changes in the BBB and increased transcellular permeability that showed regional heterogeneity in its responses. Moreover, NMDA receptor activation increased endosomal trafficking and facilitated inactivation of lysosomal pathways and consequently increased molecular delivery mediated by activation of calmodulin-dependent protein kinase II (CaMKII) and RhoA/protein kinase C (PKC). Subsequent in vivo experiments using mice specifically lacking NMDA receptor subunit 1 in endothelial cells showed decreased neuronal density in the brain cortex, suggesting that a deficiency in NMDA receptor signaling in brain endothelial cells induces neuronal losses. Together, these results highlight the importance of NMDA-receptor-mediated signaling in the regulation of BBB permeability that surprisingly also affected CD31 staining.
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연구본부 (치매 연구그룹)
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