Fine structural nature of delayed neuronal death following ischemia in the gerbil hippocampus.
An unusual, delayed neuronal death (DND) has been noticed in the hippocampus of the Mongolian gerbil following brief ischemia (Kirino 1982). On day 1 following 5--10 min of ischemia, light microscopy showed the CA1 pyramidal cells unchanged. On day 2, the cells showed massive growth of membranous cytoplasmic organelles instead of overt cellular disintegration. These neurons were destroyed extensively by day 4 after ischemic insult. Following longer ischemia (20--30 min), however, the changes in the CA1 pyramidal cells appeared faster and resembled the well-characterized ischemic cell change (ICC). To further clarify the differences between ICC and DND, gerbils were submitted to transient 5--30 min ischemia. They were perfusion-fixed following a given survival period and then processed for electron microscopy. Following transient ischemia, specimens showed slow cell changes with growth of cisterns of the endoplasmic reticulum (ER). In some CA1 neurons, the cytoplasm was shrunken and darkly stained, but they also displayed accumulation of ER cisterns. Occasionally, the CA1 cells demonstrated highly shrunken dark perikarya, no different than in ICC. These results indicate that DND seems to be the typical disease process of the CA1 sector and that a severer insult makes the change faster and more similar to ICC. ICC seems to occur when the CA1 pyramidal cells are damaged so severely that they cannot react with proliferous activity.
D000818:Animals; D002470:Cell Survival; D004721:Endoplasmic Reticulum / Q000648:ultrastructure; D006624:Hippocampus / Q000473:pathology*; D002546:Ischemic Attack, Transient / Q000473:pathology*; D008297:Male; D008854:Microscopy, Electron; D009474:Neurons / Q000648:ultrastructure*; D012270:Ribosomes / Q000648:ultrastructure; D013997:Time Factors