Delayed neuronal death in the gerbil hippocampus following ischemia.
In the CA1 subfield of the gerbil hippocampus, an unusual series of changes were noticed after ischemia. Mongolian gerbils were subjected to bilateral carotid occlusion for 5 min. Perfusion fixation was performed 3, 6 and 12 h or 1, 2, 4, 7 and 21 days afterwards. Specimens obtained from the dorsal hippocampus were processed for light and electron microscopy. Three different types of changes were observed in the CA4, CA2 and CA1 subfields. In CA4, the change was rapid and corresponded to ischemic cell change. The alteration in CA2 was relatively slow, and identical to what has been called reactive change. On the contrary, the change in the CA1 pyramidal cells was very slow, only becoming apparent by light microscopy 2 days following ischemia. The CA1 subfield was selected for electron microscopic observation. The lamellar alignment of proliferated cisterns of the endoplasmic reticulum was the most conspicuous finding in these cells. Four days following ischemia, almost all of the pyramidal cells in CA1 were destroyed. In the CA1 neuropil, numerous presynaptic terminals remained without being apposed to normal postsynaptic sites. These changes in CA1, called here 'delayed neuronal death', may differ from those thought to be typical of ischemic neuronal damage. It was unlikely that the disturbance of local blood vessels was the cause of these changes.
D000818:Animals; D002545:Brain Ischemia / Q000503:physiopathology*; D002339:Carotid Arteries / Q000502:physiology; D003712:Dendrites / Q000648:ultrastructure; D004721:Endoplasmic Reticulum / Q000648:ultrastructure; D005849:Gerbillinae; D006624:Hippocampus / Q000503:physiopathology* / Q000648:ultrastructure; D008854:Microscopy, Electron; D009043:Motor Activity; D009474:Neurons / Q000502:physiology* / Q000648:ultrastructure; D011712:Pyramidal Tracts / Q000503:physiopathology / Q000648:ultrastructure