Skip to main content
Fig. 3 | Fluids and Barriers of the CNS

Fig. 3

From: Blood tissue Plasminogen Activator (tPA) of liver origin contributes to neurovascular coupling involving brain endothelial N-Methyl-D-Aspartate (NMDA) receptors

Fig. 3

Endothelial NMDAR controls NVC, an effect mediated by vascular tPA. A Schematic representation of the generation of VE-Cadherin Cre/Grin-1 Lox mice. The cadherin 5 promoter was used to drive expression of CRE recombinase in the vascular endothelium. LoxP sites were flanked in the transmembrane and C-term regions of Grin-1 gene (exons 11–21). This configuration carries out the deletion of endothelial Grin-1 gene while conserving Grin-1 in other cells. B Schematic representation of the experimental timeline of whisker stimulation paradigm: 3 trains of stimulations were made on laser speckle flowmetry before IV infusion of rtPA for 10 min and 3 additional trains after (control group corresponds to an IV infusion of HEPES buffer). C Colormap corresponds to the activation map related ∆CBF changes during whisker stimulations in VECad-CreΔGluN1 mice and their littermate before and after IV infusion of rtPA. Warm colours indicate an elevation of CBF during whisker stimulations. D, E Time course of % CBF increase (mean ± SEM) during whisker stimulations () in VECad-CreΔGluN1 mice (E) and their littermate (D), before (/) and after (/) IV infusion of rtPA. F Box plots show the variations of % CBF increase from baseline during whisker stimulations in VECad-CreΔGluN1 mice and their wild type littermates before and after IV infusions of rtPA. Box plots with medians, 1st and 3rd quartiles, min and max with values for each mouse. *p < 0.05 from VECad-CreWT or -rtPA, Kruskal–Wallis and Uncorrected Dunn’s tests, n = 8 VECad-CreWT, n = 10 VECad-CreΔGluN1

Back to article page