scholarly journals Valeriana officinalis Extracts Ameliorate Neuronal Damage by Suppressing Lipid Peroxidation in the Gerbil Hippocampus Following Transient Cerebral Ischemia

2015 ◽  
Vol 18 (6) ◽  
pp. 642-647 ◽  
Author(s):  
Dae Young Yoo ◽  
Hyo Young Jung ◽  
Sung Min Nam ◽  
Jong Whi Kim ◽  
Jung Hoon Choi ◽  
...  
Keyword(s):  
Lipid Peroxidation ◽  
Cerebral Ischemia ◽  
Neuronal Damage ◽  
Transient Cerebral Ischemia ◽  
Valeriana Officinalis

scholarly journals Accelerated and Exacerbated Effects of High Dietary Fat on Neuronal Damage Induced by Transient Cerebral Ischemia in the Gerbil Septum

2014 ◽  
Vol 29 (3) ◽  
pp. 328 ◽  
Author(s):  
Seung Hwan Cheon ◽  
Bing Chun Yan ◽  
Bai Hui Chen ◽  
Joon Ha Park ◽  
Ji Hyeon Ahn ◽  
...  
Keyword(s):  
Cerebral Ischemia ◽  
Dietary Fat ◽  
Neuronal Damage ◽  
Transient Cerebral Ischemia

scholarly journals Postischemic Blockade of AMPA but Not NMDA Receptors Mitigates Neuronal Damage in the Rat Brain following Transient Severe Cerebral Ischemia

1992 ◽  
Vol 12 (1) ◽  
pp. 2-11 ◽  
Author(s):  
B. Nellgård ◽  
T. Wieloch
Keyword(s):  
Cerebral Ischemia ◽  
Nmda Receptor ◽  
Ampa Receptor ◽  
Neuronal Damage ◽  
Transient Cerebral Ischemia ◽  
Coupled Processes ◽  
Temporal Part ◽  
Nmda Receptor Antagonists ◽  
Receptor Antagonists ◽  
Cgp 40116

Glutamatergic transmission is an important factor in the development of neuronal death following transient cerebral ischemia. In this investigation the effects of N-methyl-d-aspartate (NMDA) and non-NMDA receptor antagonists on neuronal damage were studied in rats exposed to 10 min of transient cerebral ischemia induced by bilateral common carotid occlusion combined with hypotension. The animals were treated with a blocker of the ionotropic quisqualate or α-amino-3-hydroxy-5-methyl-4-isoxazole (AMPA) receptor, 2.3-dihydroxy-6-nitro-7-sulfamoyl-benzo( F)quinoxaline (NBQX), given postischemia as an intraperitoneal bolus dose of 30 mg kg−1 followed by an intravenous infusion of 75 μg min−1 for 6 h, or with the noncompetitive NMDA receptor blocker dizocilpine(MK-801) given 1 mg kg−1 i.p. at recirculation and 3 h postischemia, or with the competitive NMDA receptor antagonist dl-( E)-2-amino-4-methyl-5-phosphono-3-pentenoic acid (CGP 40116), 5 mg kg−1, given intraperitoneally at recirculation. Treatment with NBQX provided a significant reduction of neuronal damage in the hippocampal CA1 area by 44–69%, with the largest relative decrease in the temporal part of the hippocampus. In neocortex a significant decrease in the number of necrotic neurons was also noted. No protection could be seen following postischemic treatment with dizocilpine or CGP 40116. Our data demonstrate that AMPA but not NMDA receptor antagonists decrease neuronal damage following transient severe cerebral ischemia in the rat and that the protection by NBQX may be dependent on the severity of the ischemic insult. We propose that the AMPA receptor–mediated neurotoxicity could be due to ischemia-induced changes in the control mechanisms of AMPA receptor–coupled processes or to changes of AMPA receptor characteristics.

Neuronal Damage Using Fluoro-Jade B Histofluorescence and Gliosis in the Striatum After Various Durations of Transient Cerebral Ischemia in Gerbils

2012 ◽  
Vol 37 (4) ◽  
pp. 826-834 ◽  
Author(s):  
Taek Geun Ohk ◽  
Ki-Yeon Yoo ◽  
Seung Min Park ◽  
Bich Na Shin ◽  
In Hye Kim ◽  
...  
Keyword(s):  
Cerebral Ischemia ◽  
Neuronal Damage ◽  
Transient Cerebral Ischemia ◽  
Fluoro Jade B

Neuronal damage and gliosis in the somatosensory cortex induced by various durations of transient cerebral ischemia in gerbils

2013 ◽  
Vol 1510 ◽  
pp. 78-88 ◽  
Author(s):  
Jae-Chul Lee ◽  
Ji Hyeon Ahn ◽  
Dae Hwan Lee ◽  
Bing Chun Yan ◽  
Joon Ha Park ◽  
...  
Keyword(s):  
Cerebral Ischemia ◽  
Somatosensory Cortex ◽  
Neuronal Damage ◽  
Transient Cerebral Ischemia

scholarly journals Changes in Insulin-like Growth Factor 1 Receptor Density after Transient Cerebral Ischemia in the Rat. Lack of Protection against Ischemic Brain Damage following Injection of Insulin-Like Growth Factor 1

1993 ◽  
Vol 13 (5) ◽  
pp. 895-898 ◽  
Author(s):  
Kerstin Bergstedt ◽  
Tadeusz Wieloch
Keyword(s):  
Cerebral Ischemia ◽  
Growth Factor ◽  
Neuronal Damage ◽  
Brain Slices ◽  
Transient Cerebral Ischemia ◽  
Insulin Like Growth Factor ◽  
Vessel Occlusion ◽  
Ischemic Brain ◽  
Intracerebroventricular Injections ◽  
Intracellular Signal

Binding of 125I-insulin-like growth factor-1 (125I-IGF-1) to rat brain slices was studied after 15 min of two-vessel occlusion ischemia and 1 h to 4 days of recirculation. Ligand binding in the hippocampus increased at 6 h post ischemia in the CA1 and CA3 regions and the dentate gyrus, suggesting that the IGF-1 receptors were up-regulated, while no change was seen in neocortex and striatum. Intracerebroventricular injections of IGF-1 (2 μg) prior to and after transient cerebral ischemia did not reduce neuronal damage. The increased up-regulation on IGF-1 receptors and the absence of neuroprotection by IGF-1 suggest that the intracellular signal transduction chain activated by the IGF-1 receptor may be interrupted.

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