Amyloid-β disrupts unitary calcium entry through endothelial NMDA receptors in mouse cerebral arteries.

ABSTRACT: Transient increases in intracellular Ca²⁺ activate endothelium-dependent vasodilatory pathways. This process is impaired in cerebral amyloid angiopathy, where amyloid-β_(1-40) accumulates around blood vessels. In neurons, amyloid-β impairs the Ca²⁺-permeable N-methyl-D-aspartate receptor (NMDAR), a mediator of endothelium-dependent dilation in arteries. We hypothesized that amyloid-β_(1-40) reduces NMDAR-elicited Ca²⁺ signals in mouse cerebral artery endothelial cells, blunting dilation. Cerebral arteries isolated from 4-5 months-old, male and female cdh5:Gcamp8 mice were used for imaging of unitary Ca²⁺ influx through NMDAR (NMDAR sparklets) and intracellular Ca²⁺ transients. The

SUBMITTER: Peters EC 

PROVIDER: S-EPMC8721780 | biostudies-literature | 2022 Jan

REPOSITORIES: biostudies-literature