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. 2015 Jan 28;35(5):818–827. doi: 10.1038/jcbfm.2014.255

Figure 2.

Figure 2

Infarct area and albumin extravasation after neonatal hypoxia-ischemia (HI). (A) Illustrations of MAP-2 and albumin immunoreactivity in tissue sections after HI. MAP-2 was used to delineate the infarct area and albumin was used to detect areas with compromised blood–brain barrier function to larger proteins. At 2 hours after HI, MAP-2 immunoreactivity was reduced in hippocampus in all animals and also in thalamus in some animals. With time MAP-2 staining was also lost in cortex (6 and 24 hours). Albumin was detected in hippocampus in some animals at 2 hours (4/5 animals). At 6 and 24 hours albumin was detected in hippocampus in all animals and sometimes also in thalamus and cortex. The albumin-positive area was always contained within the MAP-2-negative area and at 24 hours these two areas were almost identical in all animals. Scale bar is 1 mm. (B) Measurements of MAP-2-negative and albumin-positive areas of the brain sections. Measurements were made in two hippocampal sections from each animal and averaged. Both areas increased with time after HI. Data are mean±s.e.m., n=5/group; *P<0.05 (t-test). (C) Correlation of MAP-2-negative and Albumin-positive area across all animals and time points. There was a linear correlation of these two areas with almost identical slopes at 6 and 24 hours after HI.