Delayed neuronal death prevented by inhibition of increased hydroxyl radical formation in a transient cerebral ischemia

1997 ◽  
Vol 762 (1-2) ◽  
pp. 240-242 ◽  
Author(s):  
Toshihiro Yamamoto ◽  
Satoshi Yuki ◽  
Toshiaki Watanabe ◽  
Masayuki Mitsuka ◽  
Ken-Ichi Saito ◽  
...  
Keyword(s):  
Cerebral Ischemia ◽  
Hydroxyl Radical ◽  
Neuronal Death ◽  
Transient Cerebral Ischemia ◽  
Radical Formation ◽  
Delayed Neuronal Death

scholarly journals Induction of Caspase-3-Like Protease May Mediate Delayed Neuronal Death in the Hippocampus after Transient Cerebral Ischemia

1998 ◽  
Vol 18 (13) ◽  
pp. 4914-4928 ◽  
Author(s):  
Jun Chen ◽  
Tetsuya Nagayama ◽  
Kunlin Jin ◽  
R. Anne Stetler ◽  
Raymond L. Zhu ◽  
...  
Keyword(s):  
Cerebral Ischemia ◽  
Neuronal Death ◽  
Caspase 3 ◽  
Transient Cerebral Ischemia ◽  
Delayed Neuronal Death

scholarly journals Protein Ubiquitination in Postsynaptic Densities after Transient Cerebral Ischemia

2004 ◽  
Vol 24 (11) ◽  
pp. 1219-1225 ◽  
Author(s):  
Chen Li Liu ◽  
Maryann E. Martone ◽  
Bingren R. Hu
Keyword(s):  
Cerebral Ischemia ◽  
Neuronal Death ◽  
Structural Damage ◽  
Ubiquitin Proteasome System ◽  
Transient Cerebral Ischemia ◽  
Delayed Neuronal Death ◽  
Western Blots ◽  
Ca1 Region ◽  
Protein Ubiquitination ◽  
Neurologic Deficits

The mechanisms underlying neurologic deficits and delayed neuronal death after ischemia are not fully understood. In the present study, we report that transient cerebral ischemia induces accumulation of ubiquitinated proteins (ubi-proteins) in postsynaptic densities (PSDs). By immunoelectron microscopy, we demonstrated that ubi-proteins were highly accumulated in PSD structures after ischemia. On Western blots, ubi-proteins were markedly increased in purified PSDs at 30 minutes of reperfusion, and the increase persisted until cell death in the CA1 region after ischemia. In the resistant DG area, however, the changes were transient and significantly less pronounced. Deposition of ubi-proteins in PSDs after ischemia correlates well with PSD structural damage in the CA1 region as viewed by electron microscopy. These results suggest that the ubiquitin-proteasome system fails to repair and remove damaged proteins in PSDs. The changes may demolish synaptic neurotransmission, contribute to neurologic deficits, and eventually lead to delayed neuronal death after transient cerebral ischemia.

Immunohistochemical investigation of caspase-1 and effect of caspase-1 inhibitor in delayed neuronal death after transient cerebral ischemia

2001 ◽  
Vol 893 (1-2) ◽  
pp. 113-120 ◽  
Author(s):  
Yasuhito Hayashi ◽  
Ikuyo Jikihara ◽  
Takashi Yagi ◽  
Masayuki Fukumura ◽  
Yuichi Ohashi ◽  
...  
Keyword(s):  
Cerebral Ischemia ◽  
Neuronal Death ◽  
Transient Cerebral Ischemia ◽  
Delayed Neuronal Death ◽  
Immunohistochemical Investigation ◽  
Caspase 1

Transient Cerebral Ischemia Induces Active Astrocytosis Without Distinct Neuronal Death in the Gerbil Main Olfactory Bulb: A Long-Term Analysis

2010 ◽  
Vol 35 (10) ◽  
pp. 1588-1598 ◽  
Author(s):  
Jung Hoon Choi ◽  
Ki-Yeon Yoo ◽  
Choong Hyun Lee ◽  
Ok kyu Park ◽  
Bing Chun Yan ◽  
...  
Keyword(s):  
Cerebral Ischemia ◽  
Olfactory Bulb ◽  
Neuronal Death ◽  
Transient Cerebral Ischemia ◽  
Main Olfactory Bulb ◽  
Term Analysis
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