Representative photomicrographs of immunostaining after transient brainstem ischemia for 15 min (pons). 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 MAP2 staining were detected in the lateral vestibular nucleus (LVe: B; blue arrows) and the ventral part of the spinal trigeminal nucleus (Sp5: B; red arrows) after bilateral vertebral artery occlusion (BVO) for 15 min. These ischemic lesions had disappeared at 1 day after reperfusion (C). At 3 days and 7 days after reperfusion, ischemic lesions appeared again and expanded further (D and E; blue and red arrows). New ischemic lesions were detected in the dorsal part of Sp5 (D and E; blue arrowheads) and ventral cochlear nucleus (VC) (D and E; red arrowheads). At the same time, clusters of amoeboid microglia/macrophages were detected in the same areas (I and J; blue and red arrows/arrowheads). At 3 days and 7 days after reperfusion, immunoreactivity for GFAP was lost in the ischemic lesions, and increased immunoreactivity for GFAP was detected around ischemic lesions (N and O; blue and red arrows/arrowheads). Scale bar = 1 mm.
Cao et al. BMC Neuroscience 2010 11:115 doi:10.1186/1471-2202-11-115