Figure 3.

Representative photomicrographs of immunostaining after transient brainstem ischemia for 15 min (spinal trigeminal nucleus). Left column shows immunoreactivity for MAP2 (A-E); middle column shows immunoreactivity for IBA-1 (F-J); right column shows immunoreactivity for GFAP (K-O). Ischemic lesions with loss of immunoreactivity for MAP2 were seen in the ventral part of Sp5 after bilateral vertebral artery occlusion (BVO) for 15 min (B; red arrows), and these lesions had disappeared at 1 day after reperfusion (C). However, ischemic lesions had reappeared and expanded further (D and E; red arrows) and new ischemic lesions were detected in the dorsal part of Sp5 (D and E; blue arrowheads) at 3 days and 7 days after reperfusion. Clusters of IBA-1-positive amoeboid microglia/macrophages (I and J; red arrows and blue arrowheads) and loss of GFAP expression (N and O; red arrows and blue arrowheads) were detected in the same areas where MAP2 expression was lost at 3 days and 7 days after reperfusion. Increased immunoreactivity for GFAP (N and O; red arrows and blue arrowheads) was also detected around ischemic lesions at 3 days and 7 days after reperfusion. Scale bars = 0.5 mm.

Cao et al. BMC Neuroscience 2010 11:115   doi:10.1186/1471-2202-11-115
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