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. Author manuscript; available in PMC: 2009 Oct 5.
Published in final edited form as: J Cereb Blood Flow Metab. 2008 Jul 9;28(11):1771–1785. doi: 10.1038/jcbfm.2008.76

Figure 1.

Figure 1

Intravascular administration of FITC-LEA specifically binds glycoconjugates associated with the luminal glycocalyx of all perfused spinal microvessels in the normal adult mouse spinal cord. The relative hypervascularity of spinal gray matter is apparent (A; gray matter is outlined with dashed line). The specific interaction of FITC-LEA with spinal ECs is apparent in high-magnification insets (C to H). No colocalization of FITC-LEA is observed with neuronal elements (C), astrocytes (D), or oligodendrocytes (E) as shown by immunoreactivity for Map2, GFAP, or OSP, respectively. Conversely, double labeling of FITC-LEA with the vascular EC markers PECAM-1 (F; arrows), Glut-1 (G; arrows), and claudin-5 (H; arrows) is apparent. The specificity of the interaction between FITC-LEA and the glycocalyx of spinal vascular ECs is further shown by a lack of microvascular labeling when a molecular-weight-matched FITC-dextran is administered intravascularly (B; gray/white matter boundary indicated by the dashed line). Scale bars = 500 μm (A); 250 μm (B); 50 μm (C to H).