Selective Vulnerability and Early Progression of Hippocampal CA1 Pyramidal Cell Degeneration and GFAP-Positive Astrocyte Reactivity in the Rat Four-Vessel Occlusion Model of Transient Global Ischemia

1993 ◽  
Vol 119 (1) ◽  
pp. 128-139 ◽  
Author(s):  
J.M. Ordy ◽  
T.M. Wengenack ◽  
P. Bialobok ◽  
P.D. Coleman ◽  
P. Rodier ◽  
...  
Keyword(s):  
Pyramidal Cell ◽  
Selective Vulnerability ◽  
Global Ischemia ◽  
Cell Degeneration ◽  
Vessel Occlusion ◽  
Hippocampal Ca1 ◽  
Occlusion Model ◽  
Early Progression ◽  
Transient Global Ischemia

scholarly journals Mouse Transient Global Ischemia Two-Vessel Occlusion Model

BIO-PROTOCOL ◽  
2012 ◽  
Vol 2 (18) ◽  
Author(s):  
Fabrizio Pontarelli ◽  
Dimitry Ofengeim ◽  
R. Zukin ◽  
Elizabeth Jonas
Keyword(s):  
Global Ischemia ◽  
Vessel Occlusion ◽  
Occlusion Model ◽  
Transient Global Ischemia

Visfatin reduces hippocampal CA1 cells death and improves learning and memory deficits after transient global ischemia/reperfusion

Neuropeptides ◽  
2015 ◽  
Vol 49 ◽  
pp. 63-68 ◽  
Author(s):  
Sohaila Erfani ◽  
Mehdi Khaksari ◽  
Shahrbanoo Oryan ◽  
Nabi Shamsaei ◽  
Nahid Aboutaleb ◽  
...  
Keyword(s):  
Learning And Memory ◽  
Ischemia Reperfusion ◽  
Memory Deficits ◽  
Global Ischemia ◽  
Hippocampal Ca1 ◽  
Transient Global Ischemia ◽  
Learning And Memory Deficits ◽  
Cells Death ◽  
Ca1 Cells

[D-Ala2, D-Leu5]-Enkephalin (Dadle) Reduces Inflammation Responses after Transient Global Ischemia

2011 ◽  
Vol 345 ◽  
pp. 343-348
Author(s):  
Shu Yan Wang ◽  
Ya Le Duan ◽  
Qing Wen Zeng ◽  
Zheng Zhao ◽  
Xiang Rui Wang
Keyword(s):  
Neuronal Loss ◽  
Brain Regions ◽  
Global Ischemia ◽  
Single Infusion ◽  
Vessel Occlusion ◽  
Ischemic Brain ◽  
Transient Global Ischemia ◽  
Δ Opioid Receptor ◽  
The Right ◽  
Inflammation Responses

[D-Ala2, D-Leu5]-Enkephalin (DADLE) is a δ-opioid receptor antagonist and has been shown to reduce neuronal loss in the selectively vulnerable brain regions after transient global ischemia. Here, we investigate whether this protection is mediated by the DADLE's modulation of the postischemia inflammation responses. After implanted with cannula at the right lateral ventricle, rats underwent 10 minutes of transient global ischemia by four vessel occlusion. Rats received a single infusion of DADLE (12.5 nmol) via the intracerebral cannula at the onset of reperfusion. At the time of 72 h after ischemia, we investigated GFAP expression via immunohistochemistry. we also tested the level of MDA and the activities of SOD and CAT. The results show that DADLE can reduce reactive astrocytosis and increase SOD activities. The study reveals the neuroprotection mechanism of DADLE in the ischemic brain is related to reduce inflammation responses.

scholarly journals Ischemic Damage in Hippocampal CA1 is Dependent on Glutamate Release and Intact Innervation from CA3

1989 ◽  
Vol 9 (5) ◽  
pp. 629-639 ◽  
Author(s):  
H. Benveniste ◽  
M. B. Jørgensen ◽  
M. Sandberg ◽  
T. Christensen ◽  
H. Hagberg ◽  
...  
Keyword(s):  
Injection Site ◽  
Glutamate Release ◽  
Pyramidal Cells ◽  
Global Ischemia ◽  
Ischemic Damage ◽  
Ca1 Pyramidal Cells ◽  
Ca1 Region ◽  
Hippocampal Tissue ◽  
Hippocampal Ca1 ◽  
Transient Global Ischemia

The removal of glutamatergic afferents to CA1 by destruction of the CA3 region is known to protect CA1 pyramidal cells against 10 min of transient global ischemia. To investigate further the pathogenetic significance of glutamate, we measured the release of glutamate in intact and CA3-lesioned CA1 hippocampal tissue. In intact CA1 hippocampal tissue, glutamate increased sixfold during ischemia; in the CA3-lesioned CA1 region, however, glutamate only increased 1.4-fold during ischemia. To assess the neurotoxic potential of the ischemia-induced release of glutamate, we injected the same concentration of glutamate into the CA1 region as is released during ischemia in normal, CA3-lesioned, and ischemic CA1 tissue. We found that this particular concentration of glutamate was sufficient to destroy CA1 pyramids in the vicinity of the injection site in intact and CA3-lesioned CA1 tissue when administered during control (non-ischemic) conditions. In contrast, the same amount injected during ischemia in the CA3-lesioned CA1 region destroyed pyramidal cells in a widely distributed zone around the injection site in the CA1 region. It is concluded that the ischemia-induced damage of pyramidal cells in CA1 is dependent on glutamate release and intact innervation from CA3.

Hippocampal CA1 cell loss in a non-human primate model of transient global ischemia: A pilot study

2007 ◽  
Vol 74 (1-3) ◽  
pp. 164-171 ◽  
Author(s):  
Koichi Hara ◽  
Takao Yasuhara ◽  
Noriyuki Matsukawa ◽  
Mina Maki ◽  
Tadashi Masuda ◽  
...  
Keyword(s):  
Pilot Study ◽  
Cell Loss ◽  
Global Ischemia ◽  
Primate Model ◽  
Hippocampal Ca1 ◽  
Transient Global Ischemia ◽  
Human Primate

scholarly journals Prolonged Therapeutic Hypothermia does not Adversely Impact Neuroplasticity after Global Ischemia in Rats

2012 ◽  
Vol 32 (8) ◽  
pp. 1525-1534 ◽  
Author(s):  
Gergely Silasi ◽  
Ana C Klahr ◽  
Mark J Hackett ◽  
Angela M Auriat ◽  
Helen Nichol ◽  
...  
Keyword(s):  
Synapse Formation ◽  
Tissue Injury ◽  
Vessel Occlusion ◽  
X Ray ◽  
Animal Data ◽  
Hippocampal Ca1 ◽  
Occlusion Model ◽  
Neurotropic Factor ◽  
Normothermic Group ◽  
Unilateral Brain

Hypothermia improves clinical outcome after cardiac arrest in adults. Animal data show that a day or more of cooling optimally reduces edema and tissue injury after cerebral ischemia, especially after longer intervention delays. Lengthy treatments, however, may inhibit repair processes (e.g., synaptogenesis). Thus, we evaluated whether unilateral brain hypothermia (∼33°C) affects neuroplasticity in the rat 2-vessel occlusion model. In the first experiment, we cooled starting 1 hour after ischemia for 2, 4, or 7 days. Another group was cooled for 2 days starting 48 hours after ischemia. One group remained normothermic throughout. All hypothermia treatments started 1 hour after ischemia equally reduced hippocampal CA1 injury in the cooled hemisphere compared with the normothermic side and the normothermic group. Cooling only on days 3 and 4 was not beneficial. Importantly, no treatment influenced neurogenesis (Ki67/Doublecortin (DCX) staining), synapse formation (synaptophysin), or brain-derived neurotropic factor (BDNF) immunohistochemistry. A second experiment confirmed that BDNF levels (ELISA) were equivalent in normothermic and 7-day cooled rats. Last, we measured zinc (Zn), which is important in plasticity, with X-ray fluorescence imaging in normothermic and 7-day cooled rats. Hypothermia did not alter the postischemic distribution of Zn within the hippocampus. In summary, cooling significantly mitigates injury without compromising neuroplasticity.

The temporal and spatial changes of actin cytoskeleton in the hippocampal CA1 neurons following transient global ischemia

2019 ◽  
Vol 1720 ◽  
pp. 146297 ◽  
Author(s):  
Chun-Yan Guo ◽  
Tian-Qing Xiong ◽  
Bai-Hong Tan ◽  
Yue Gui ◽  
Ning Ye ◽  
...  
Keyword(s):  
Actin Cytoskeleton ◽  
Global Ischemia ◽  
Ca1 Neurons ◽  
Hippocampal Ca1 Neurons ◽  
Spatial Changes ◽  
Hippocampal Ca1 ◽  
Transient Global Ischemia ◽  
Temporal And Spatial
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