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. 2017 Aug 31;76(10):898–907. doi: 10.1093/jnen/nlx074

FIGURE 1.

FIGURE 1

Upregulation of αEnsa protein in rat tMCAo is detected using a polyclonal rabbit-anti-αEnsa primary antibody. Immunofluorescence results in rat tMCAo (A) and control brain (B), using a polyclonal rabbit-anti-αEnsa primary antibody. Double label immunofluorescence reveals prominent upregulation of αEnsa protein in NeuN-positive neurons (C), GFAP-positive astrocytes (E), and rat endothelial cell antigen-1 (RECA-1) positive endothelial cells (G) in ischemic tissues versus nonischemic contralateral controls (D, F, and H, respectively); merged double label images are shown in the third and fourth columns. Quantification of αEnsa protein expression in core versus peri-infarct regions at various times after MCAo, as indicated (I); 6 rats/group; **p < 0.01; original magnification, 20× (A, B) or 40× (C–H); scale bars, 100 µm (A, B); 10 µm (C–H); αEnsa, red/CY3; NeuN, GFAP, and RECA, green/FITC; nuclei, blue/DAPI. Images shown are from specimens 24 hours after ischemia/reperfusion.