Figure 7

Infarct distribution in SDs and SHRs. Representative examples are shown of the infarct distribution after 90 minutes of tMCAo in the SD and SHR strains using NeuN and ED-1 immunohistochemistry. The ED-1 (brownish red rows) was visualized with NovaRed^®, whereas NeuN stain was developed with nickel-enhanced DAB (grey rows). A and B depict the infarct pattern we found in SDs. Usually, the infarcts were restricted to the subcortical structures in SDs encompassing both the MCA and AChA/HTA territories (4 SDs) (A) or the AChA/HTA territories alone (5 SDs) (B) Three of the tMCAo SDs had no histological signs of neuronal loss on the NeuN stain. C, D and E illustrate the infarct distribution in SHRs. In most of the SHRs subjected to ischemia the infarcted area included the neocortex (8 out of 11 SHRs). C shows an example of ischemia affecting the ACA, MCA and AChA/HTA (2 SHRs). The majority of animals had ischemia in the MCA and AChA/HTA territories (8 SHRs) (D). Only one SHR had a small ischemic lesion solely affecting the AChA/HTA territories (E). ACA, anterior cerebral artery; AChA, anterior choroidal artery; DAB, 3,3'-diaminobenzidine; HTA, hypothalamic artery; MCA, middle cerebral artery; NeuN, neuronal nuclei; SDs, Sprague-Dawley rats; SHRs, spontaneously hypertensive rats; tMCAo, transient middle cerebral artery occlusion.