Transition of areas of eosinophilic neurons and reactive astrocytes to delayed cortical infarcts after transient unilateral forebrain ischemia in Mongolian gerbils.

The fate of postischemic tissues containing eosinophilic neurons (ENs), whether they remain viable or evolve into infarction, is largely unknown. We analyzed the time profile and distribution of ENs, reactive astrocytes (RAs), and infarction after transient cerebral ischemia. Unilateral forebrain ischemia was induced in Mongolian gerbils by two 10-min unilateral common carotid artery occlusions with a 5-h interval, and the brains at 24 h, 4 days, and 2, 4, and 16 weeks were prepared for morphometric analysis. Intra-ischemic laser Doppler flowmetry revealed significant ischemia, deeper in the anterior cortex, during carotid occlusion. Here, ENs appeared in the middle and deep layers at 24 h postischemia, and EN areas had extended to all cortical layers by 4 days. Large areas of high EN density turned into infarcts between 4 days and 4 weeks. In the posterior cortex, middle and deep cortical layers evolved low EN density areas without subsequent transformation into infarcts. RAs were consistently observed in areas with ENs, and RA areas with high EN density were largely transformed into infarcts between 4 days and 4 weeks postischemia. Areas of high, but not low, EN density were slowly transformed into infarcts after transient cerebral ischemia. Delayed astrocytic death took place in the RA areas with high EN density. In conclusion, density of ENs is an important indicator of delayed astrocytic death and infarction in postischemic tissue.