Electron microscopic investigation of the cerebral cortex after cerebral ischemia and reperfusion in the gerbil.
Prompt dendritic damage has been observed in the hippocampus of the gerbil brain after transient cerebral ischemia. In the present study, we studied the frontoparietal cortex of the gerbil brain electron microscopically after brief bilateral carotid occlusion to assess the vulnerability of dendritic processes. After ischemia for 5 min, there was swelling of the periphery of dendrites accompanied by swelling of mitochondria, cytoplasmic vacuolation and disintegration of microtubules in layer I, which spread to layer III after ischemia for 20 min. After reperfusion for 3-24 h following ischemia for 20 min, swelling in the periphery of dendrites and of mitochondria inside receded but vacuole formation and disintegration of microtubules propagated proximally. In neuronal perikarya, polyribosomal disaggregation was observed after ischemia for 20 min and persisted thereafter, while fragmentation of rough endoplasmic reticulum (ER) and microvacuolation occurred after reperfusion for 3 h. Electron-dense clumping of neuronal perikarya was observed after reperfusion for 6 h particularly in layers III and Vb, which increased in number for up to 72 h. The observed progressive damage in dendrites may be common to neurons vulnerable to cerebral ischemia and may significantly contribute to development of delayed neuronal death.
Tomimoto
H
H
Department of Neurology, Mayo Clinic, Rochester, MN 55905.
Yanagihara
T
T
D000818:Animals; D005260:Female; D005625:Frontal Lobe / Q000098:blood supply / Q000648:ultrastructure*; D005849:Gerbillinae; D002546:Ischemic Attack, Transient / Q000473:pathology*; D008297:Male; D008854:Microscopy, Electron; D010296:Parietal Lobe / Q000098:blood supply / Q000648:ultrastructure*; D015427:Reperfusion Injury / Q000473:pathology*