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. Author manuscript; available in PMC: 2011 Jun 1.
Published in final edited form as: Neuroimage. 2010 Mar 4;51(2):599–605. doi: 10.1016/j.neuroimage.2010.02.073

Fig. 3.

Fig. 3

Ischemia, neuroinflammation and NMDAR distribution 30 days after MCAO.

A = Infarction (hyperintense area) shown by T2W-MRI, B =cresyl violet stained section C= Distribution of PBR labeled with [3H] PK11195, D= Distribution of NMDAR labeled with [3H] MK801, E = Non-specific binding of [3H] MK801 in the presence of excess unlabeled MK801, same anatomical level as A-D. Autoradiograms were pseudocolored using the rainbow spectrum, Max = Maximum and MIN = Minimum.

Normal distribution patterns of PBR and NMDAR are illustrated in figure 2 above. Note the presence of atrophy in the ipsilateral hemisphere at this late time point (enlarged ventricle and smaller area of the ipsilateral hemisphere), with a persistent intense increase in PBR and persistent decrease in NMDAR which is most pronounced in areas of the ipsilateral cortex where PBR density is highest.