Neuronal injury in the infarct border: a neuropathological study in the rat.
Focal ischemia was induced in rats by occlusion of the middle cerebral artery (MCA). Infarction developed primarily in the basal ganglia. The development, density and distribution of neuronal injury in the cortex adjacent to the infarct were studied from 4 h to 1 year after occlusion of the artery. The brains were perfusion fixed, sub-serially sectioned, and stained with H + E, acid fuchsin/cresyl violet, and ad modum Klüver-Barrera. The number of injured neurons was assessed by direct visual counting. Four hours after the artery occlusion, the infarct was clearly outlined in the corpus striatum, whereas the cortical border became sharp 1 to 2 days after ligation of MCA. After 1 day triangular injured neurons with eosinophilic cytoplasm and pyknotic nuclei were seen outside the infarct. The number of injured neurons at day 1, 2, 3, 4, and 5 was the same, i.e. no evidence for delayed neuronal death was found. Neuron counts at day 1, 4, 10, 17, 27, and 365 were reduced according to the number of acutely injured neurons. Most injured neurons were observed less than 3 mm from the margin of the infarct and the greatest number was found in the cortical layers 2 and 3. The border zone in the medial part of the striatum showed selective neuronal necrosis only in a zone of 200 micron. The fact that the number of injured neurons was constant from day 1 to 5 after artery occlusion indicates that the damage is acute and that a delayed loss of neurons is of minor significance.
D000818:Animals; D001479:Basal Ganglia / Q000473:pathology; D002452:Cell Count; D002540:Cerebral Cortex / Q000473:pathology*; D002544:Cerebral Infarction / Q000209:etiology / Q000473:pathology*; D002546:Ischemic Attack, Transient / Q000150:complications; D008297:Male; D009474:Neurons / Q000473:pathology*; D051381:Rats; D011919:Rats, Inbred Strains; D013997:Time Factors