scholarly journals Temporary Focal Cerebral Ischemia Results in Swollen Astrocytic End-Feet That Compress Microvessels and Lead to Focal Cortical Infarction

2010 ◽  
Vol 31 (1) ◽  
pp. 328-338 ◽  
Author(s):  
Umeo Ito ◽  
Yoji Hakamata ◽  
Emiko Kawakami ◽  
Kiyomitsu Oyanagi
Keyword(s):  
Cerebral Cortex ◽  
Cerebral Ischemia ◽  
Microvascular Obstruction ◽  
Focal Cerebral Ischemia ◽  
Abrupt Onset ◽  
Stroke Index ◽  
Neuronal Necrosis ◽  
Temporary Ischemia ◽  
Electron Microscopical ◽  
Cut Surface

We examined the mechanisms underlying the abrupt onset of the focal infarction in disseminated selective neuronal necrosis (DSNN) after temporary ischemia. Stroke-positive animals were selected according to their stroke-index score during the first 10 minutes after left carotid occlusion performed twice at a 5-hour interval. The animals were euthanized at various times after the second ischemia. Light- and electron-microscopical studies were performed chronologically on the coronal-cut surface of the cerebral cortex at the chiasmatic level, where focal infarction evolved in the maturing DSNN. We counted the number of neurons, astrocytes, and astrocytic processes (APs); measured the areas of end-feet and astrocytes; and counted the numbers of obstructed microvessels and carbon-black-suspension-perfused microvessels (CBSPm). Between 0.5 and 5 hours after ischemia, DSNN matured, with the numbers of degenerated and dead neurons increasing, and those of APs cut-ends decreasing; whereas the area of the end-feet and the numbers of obstructed microvessels increased and those of CBSPm decreased. At 12 and 24 hours after ischemia, the infarction evolved, with the area of end-feet and astrocytic number decreased; whereas the numbers of obstructed microvessels decreased and the CBSPm number increased. The focal infarction evolved by temporary microvascular obstruction because of compression by swollen end-feet.

Focal cerebral ischemia induces CRH mRNA in rat cerebral cortex and amygdala

Neuroreport ◽  
1995 ◽  
Vol 6 (13) ◽  
pp. 1785-1788 ◽  
Author(s):  
Ma-Li Wong ◽  
Sara A. Loddick ◽  
Peter B. Bongiorno ◽  
Philip W. Gold ◽  
Nancy J. Rothwell ◽  
...  
Keyword(s):  
Cerebral Cortex ◽  
Cerebral Ischemia ◽  
Focal Cerebral Ischemia ◽  
Rat Cerebral Cortex

scholarly journals Induction of Type 2 Iodothyronine Deiodinase in Astrocytes after Transient Focal Cerebral Ischemia in the Rat

2005 ◽  
Vol 25 (4) ◽  
pp. 468-476 ◽  
Author(s):  
Isabelle Margaill ◽  
Julien Royer ◽  
Dominique Lerouet ◽  
Martine Ramaugé ◽  
Claude Le Goascogne ◽  
...  
Keyword(s):  
Cerebral Cortex ◽  
Cerebral Ischemia ◽  
Thyroid Hormones ◽  
Focal Cerebral Ischemia ◽  
Iodothyronine Deiodinase ◽  
Reverse Transcription Pcr ◽  
Transient Focal Cerebral Ischemia ◽  
Ipsilateral Striatum ◽  
Future Work

This study investigated the expression of deiodinases of thyroid hormones in the rat brain after transient occlusion of the middle cerebral artery. The activity of type 2 deiodinase (D2), which catalyzes the deiodination of thyroxine into the more active thyroid hormone 3,5,3′-triiodothyronine, was strongly increased by cerebral ischemia at 6 and 24 hours in the striatum and at 24 hours in the cerebral cortex. The activity of type 3 deiodinase, which catalyzes the inactivation of thyroid hormones, was not affected by ischemia. In situ hybridization showed, as soon as 6 hours, an upregulation of the expression of D2 mRNA in the ipsilateral striatum, which disappeared at 24 hours. In the ipsilateral cortex, the induction of D2 mRNA started at 6 hours, was increased at 24 hours and finally declined at 72 hours. These results were confirmed by reverse transcription-PCR for D2 mRNA in the striatum and cerebral cortex. The upregulation of D2 mRNA after ischemia was mainly localized in astrocytic cell bodies. These results show that D2 is rapidly induced in astrocytes after ischemic stroke. Future work will include the exploration of the role of the upregulation of this enzyme, responsible for local 3,5,3′-triiodothyronine production as a neuroprotective mechanism in the brain.

scholarly journals Chronic nicotine exposure exacerbates transient focal cerebral ischemia-induced brain injury

2016 ◽  
Vol 120 (3) ◽  
pp. 328-333 ◽  
Author(s):  
Chun Li ◽  
Hong Sun ◽  
Denise M. Arrick ◽  
William G. Mayhan
Keyword(s):  
Cerebral Cortex ◽  
Brain Injury ◽  
Cerebral Ischemia ◽  
Infarct Size ◽  
Focal Cerebral Ischemia ◽  
Neurological Deficits ◽  
Control Group ◽  
Nicotine Exposure ◽  
Chronic Nicotine ◽  
Transient Focal Cerebral Ischemia

Tobacco smoking is a risk factor contributing to the development and progression of ischemic stroke. Among many chemicals in tobacco, nicotine may be a key contributor. We hypothesized that nicotine alters the balance between oxidant and antioxidant networks leading to an increase in brain injury following transient focal cerebral ischemia. Male Sprague-Dawley were treated with nicotine (2 or 4 mg·kg−1·day−1) for 4 wk via an implanted subcutaneous osmotic minipump and subjected to a 2-h middle cerebral artery occlusion (MCAO). Infarct size and neurological deficits were evaluated at 24 h of reperfusion. Superoxide levels were determined by lucigenin-enhanced chemiluminescence. Expression of oxidant and antioxidant proteins was measured using Western blot analysis. We found that chronic nicotine exposure significantly increased infarct size and worsened neurological deficits. In addition, nicotine significantly elevated superoxide levels of cerebral cortex under basal conditions. Transient focal cerebral ischemia produced an increase in superoxide levels of cerebral cortex in control group, but no further increase was found in the nicotine group. Furthermore, chronic nicotine exposure did not alter protein expression of NADPH oxidase but significantly decreased MnSOD and uncoupling protein-2 (UCP-2) in the cerebral cortex and cerebral arteries. Our findings suggest that nicotine-induced exacerbation in brain damage following transient focal cerebral ischemia may be related to a preexisting oxidative stress via decreasing of MnSOD and UCP-2.

A new model of transient focal cerebral ischemia for inducing selective neuronal necrosis

2009 ◽  
Vol 78 (4-5) ◽  
pp. 226-231 ◽  
Author(s):  
Ethem Murat Arsava ◽  
Gunfer Gurer ◽  
Yasemin Gursoy-Ozdemir ◽  
Hulya Karatas ◽  
Turgay Dalkara
Keyword(s):  
Cerebral Ischemia ◽  
Focal Cerebral Ischemia ◽  
Neuronal Necrosis ◽  
New Model ◽  
Transient Focal Cerebral Ischemia

Alterations in the N-Methyl-D-Aspartate Receptor Complex following Focal Cerebral Ischemia

1989 ◽  
Vol 9 (5) ◽  
pp. 709-712 ◽  
Author(s):  
D. Dewar ◽  
M. C. Wallace ◽  
A. Kurumaji ◽  
J. McCulloch
Keyword(s):  
Cerebral Cortex ◽  
Cerebral Ischemia ◽  
Focal Cerebral Ischemia ◽  
Artery Occlusion ◽  
Receptor Complex ◽  
Ischemic Insult ◽  
Mk 801 ◽  
Aspartate Receptor ◽  
Cerebral Artery Occlusion ◽  
The Brain

The functional integrity of the N-methyl-d-aspartate receptor complex following focal cerebral ischemia in the rat has been examined at a time when brain tissue is irreversibly damaged. Twelve hours after unilateral permanent middle cerebral artery occlusion, [3H]-MK-801 binding was not significantly altered in the ischemic cerebral cortex compared to sham-operated animals. Moreover, the enhancement of [3H]MK-801 binding by exogenous glutamate was preserved in an area of the brain that was permanently damaged by the ischemic insult.

Optimal blood glucose levels while using insulin to minimize the size of infarction in focal cerebral ischemia

2004 ◽  
Vol 101 (4) ◽  
pp. 664-668 ◽  
Author(s):  
Chang Z. Zhu ◽  
Roland N. Auer
Keyword(s):  
Blood Glucose ◽  
Cerebral Ischemia ◽  
Blood Sugar ◽  
Focal Cerebral Ischemia ◽  
Neuronal Necrosis ◽  
Content Type ◽  
Glucose Levels ◽  
Blood Glucose Levels ◽  
Cerebral Necrosis ◽  
Fine Print

Object. Insulin has been shown to ameliorate cerebral necrosis in global and, more recently, in focal cerebral ischemia. The goal of this study was to determine the relationship between this neuroprotective effect and blood sugar levels in a rat model of focal ischemia. Methods. Thirty-four rats were subjected to 80 minutes of transient middle cerebral artery occlusion at a mean arterial blood pressure of 60 mm Hg and a temperature of 37°C. Insulin (3.5 IU/kg) was administered 1 hour before (12 rats) and 20 minutes after (12 rats) ischemia; 10 animals served as controls. A quantitative histopathological study conducted after 1 week of survival showed that insulin was not beneficial in reducing the size of the infarction or selective neuronal necrosis in the penumbra when administered before or after ischemia. In addition to infarction, six animals from the insulin-treated groups had bilateral selective neuronal necrosis in the hippocampus or the neocortex. A nonlinear regression analysis in which glucose levels were compared with both cortical necrosis and total infarction yielded a U-shaped curve with a nadir for cerebral necrosis that lay in the 6- to 7-mM blood glucose range. The increased brain damage induced by insulin occurred in animals with very low blood sugar values in the range of 2 to 3 mM. Conclusions. These results in rats indicate that if insulin is used following ischemia, blood glucose levels should be maintained at approximately 6 to 7 mM. From these data one can infer that hypoglycemia of less than 3 mM should be avoided in situations of focal cerebral ischemia in which insulin is used. Additional animal studies and clinical trials in humans are needed to study the effects of insulin on ischemia.

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