Histological (thionine) and immunohistochemical (MAP2, HSP72, HSP27) characterizations of infarcts induced by a transient (30 and 120 min) and permanent MCAO.

<p>Occlusion of the MCA for 30 min always leads to an irreversible injury (infarct core) in the striatum and frequently in parts of the neocortex. The neocortex is also part of the perilesional region which also might include hippocampus, amygdala, thalamus, and hypothalamus. An irregular impairment of remote areas also occurs (cingulate and retrosplenial cortex, septum, and all contralateral affected regions). Following 120 min MCAO striatum, neocortex, amygdala, and hypothalamus are part of the infarct core. Impaired perilesional zones include hippocampus, thalamus, and hypothalamus. The ipsi- and contralateral cingulate and retrosplenial cortex and the contralateral hippocampus as well as the septal area were identified as remote affected regions. Permanent MCAO leads to infarct cores always comprising the striatum, neocortex, amygdala, and hypothalamus. Further impaired regions are similar as identified following 120 min MCAO. Rare cerebrovascular anatomies like a unilateral origin of the ACA could also lead to ischemic changes in usually remote areas like cingulate and retrosplenial cortex (1 d following 30 min MCAO). Black dotted lines indicate the infarct core and perilesional affected regions, whereas red dotted lines display remote effects. Please note that a cellular resolution can not be provided by this overview, for this purpose please refer to <a href="http://www.plosone.org/article/info:doi/10.1371/journal.pone.0004764#pone-0004764-g002" target="_blank">Fig. 2</a>. Scale bar: 2 mm.