• Y-W Ruan, X-J Han, Z-S Shi, Z-G Lei, and Z C Xu.
• Joint Laboratory for Brain Health and Function of Jinan University, The University of Hong Kong, Jinan University School of Medicine, Guangzhou 510632, China. tyiwen@jnu.edu.cn
• Neuroscience. 2012 Aug 30;218:268-77.

AbstractSynapses are essential to neuronal functions. Synaptic changes occur under physiological and pathological conditions. Here we report the remodeling of synapses in the CA1 area of the hippocampus after transient global ischemia using electron microscopy. Much electron-dense material appeared in the cytoplasm of dendrites at 24h after ischemia. Many dark axons or terminals were found in the CA1 neuropil; some of which were phagocytized by dendrites. Interestingly autophagosomes appeared in many axons or dendrites at 48 h after ischemia. In addition, postsynaptic density (PSD) - like structures or synaptic - like structures were found inside spines and dendrites. Statistical analysis demonstrated that the thickness of PSDs in the CA1 neuropil increased from 12 to 48 h after ischemia. The frequency of autophagosomes appeared to escalate from 12 to 48 h after ischemia. The frequency of asymmetric synapses was significantly increased at 12h and 24h after ischemia in stratum oriens, proximal and distal stratum radiatum. Among asymmetric synapses, the number of perforated synapses consistently increased and reached a peak (approximately 10-fold increase) at 48 h after ischemia. On the other hand, the number of multiple synaptic boutons decreased after ischemia reaching a two to fourfold decrease at 48 h after ischemia. These results have shown that ischemia induces an increase of asymmetric synapses as well as synaptic autophagy, which may contribute to the neuronal death in the CA1 area after transient global ischemia.Copyright © 2012 IBRO. Published by Elsevier Ltd. All rights reserved.

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