Figure 5: Normal cerebral microvasculature and brain glucose uptake in mutants treated early with AAV9-Glut1. | Nature Communications

Figure 5: Normal cerebral microvasculature and brain glucose uptake in mutants treated early with AAV9-Glut1.

From: Brain microvasculature defects and Glut1 deficiency syndrome averted by early repletion of the glucose transporter-1 protein

Figure 5

(a) Representative coronal images of small PET scans at 3–6 min following administration of 18F-FDG, show reduced uptake in the brain of a mutant mouse relative to WT and mutant mice treated with AAV9-Glut1. (b) Mean brain standardized uptake values (SUVs) at 3–6 min after injection of 18F-FDG in WT controls (SUV=2.2±0.11) and mutants treated with either vehicle (SUV=1.8±0.04) or AAV9-Glut1 (SUV=2.1±0.15). **, P<0.01, one-way ANOVA, N≥4 mice in each cohort. (c) Immunohistochemistry or live-imaging experimental results of the brain microvasculature of model mice administered AAV9-Glut1 depicts a capillary network that is as elaborate and dense as that of WT, control littermates. Note reduced density and fragmented aspect of the brain capillaries in all three brain regions of vehicle-treated mutants. Also note (lower panels) the fewer FITC-Dextran perfused vessels in vehicle-treated but not AAV9-Glut1-treated model mice. Graphical representations of cerebral capillary densities of the three groups of mice following an analysis of (d) 4% PFA fixed tissue or (e,f) 2-photon live-imaging experiments. ***, P<0.001, one-way ANOVA, n≥9 regions from each of N≥3 mice of each cohort.

Back to article page