Time course of microglia activation and apoptosis in various brain regions after permanent focal cerebral ischemia in mice

1998 ◽  
Vol 96 (2) ◽  
pp. 172-178 ◽  
Author(s):  
Katrin Rupalla ◽  
Peter R. Allegrini ◽  
Dirk Sauer ◽  
C. Wiessner
Keyword(s):  
Cerebral Ischemia ◽  
Time Course ◽  
Focal Cerebral Ischemia ◽  
Brain Regions ◽  
Microglia Activation

Xanthine oxidase is not a major source of free radicals in focal cerebral ischemia

1991 ◽  
Vol 260 (2) ◽  
pp. H563-H568 ◽  
Author(s):  
A. L. Betz ◽  
J. Randall ◽  
D. Martz
Keyword(s):  
Uric Acid ◽  
Free Radicals ◽  
Cerebral Ischemia ◽  
Xanthine Oxidase ◽  
Brain Edema ◽  
Focal Cerebral Ischemia ◽  
Total Activity ◽  
Brain Regions ◽  
Free Radical Scavengers ◽  
Edema Formation

Xanthine oxidase (XO) has been proposed as an important source of free radicals during ischemia. This enzyme normally exists as a dehydrogenase (XD), but it is converted to XO in some ischemic tissues. Recently, treatment of animals with the XD and XO inhibitor allopurinol or with free radical scavengers before cerebral ischemia has been shown to reduce brain injury. Therefore, we studied conversion of XD to XO in three ischemic and nonischemic brain regions during focal cerebral ischemia resulting from permanent occlusion of the middle cerebral artery (MCAO) in anesthetized rats. In nonischemic brain, 16-22% of the enzyme was in the XO form. After 24 h of ischemia this value was not significantly different (10-15%). Neither the total activity of XO nor that of XD changed, indicating that there was no irreversible conversion of XD to XO. To further explore the possible role of XO, we examined the effect of various doses of allopurinol (5, 20, or 100 mg/kg given 1 h before MCAO or 100 mg/kg given 48, 24, and 1 h before MCAO) on uric acid accumulation, brain edema formation, and cerebral blood flow (CBF) 24 h after MCAO. All but the lowest dose of allopurinol greatly reduced the appearance of uric acid in the ischemic brain; however, only the highest dose of allopurinol had any beneficial effect on brain edema. This reduction in brain edema occurred without a significant improvement in CBF. Thus XO is probably not an important source of free radicals in this model of focal cerebral ischemia.

scholarly journals MiRNA-424 Protects Against Permanent Focal Cerebral Ischemia Injury in Mice Involving Suppressing Microglia Activation

Stroke ◽  
2013 ◽  
Vol 44 (6) ◽  
pp. 1706-1713 ◽  
Author(s):  
Haiping Zhao ◽  
Jun Wang ◽  
Li Gao ◽  
Rongliang Wang ◽  
Xiangrong Liu ◽  
...  
Keyword(s):  
Cerebral Ischemia ◽  
Focal Cerebral Ischemia ◽  
Microglia Activation

Time-course of protection by the selective A2A receptor antagonist SCH58261 after transient focal cerebral ischemia

2015 ◽  
Vol 36 (8) ◽  
pp. 1441-1448 ◽  
Author(s):  
Alessia Melani ◽  
Ilaria Dettori ◽  
Francesca Corti ◽  
Lucrezia Cellai ◽  
Felicita Pedata
Keyword(s):  
Cerebral Ischemia ◽  
Receptor Antagonist ◽  
Time Course ◽  
Focal Cerebral Ischemia ◽  
Transient Focal Cerebral Ischemia ◽  
A2a Receptor

scholarly journals Cortical Neurogenesis in Adult Rats after Reversible Photothrombotic Stroke

2000 ◽  
Vol 20 (8) ◽  
pp. 1166-1173 ◽  
Author(s):  
WeiGang Gu ◽  
Thomas Brännström ◽  
Per Wester
Keyword(s):  
At Risk ◽  
Cell Proliferation ◽  
Cerebral Ischemia ◽  
Focal Cerebral Ischemia ◽  
Three Dimensional ◽  
Brain Regions ◽  
Specific Marker ◽  
Cortical Region ◽  
Adult Rats ◽  
Adult Rat

Neurogenesis occurs throughout life in the dentate gyrus of hippocampus and subventricular zone, but this phenomenon has rarely been observed in other brain regions of adult mammals. The aim of the current study was to investigate the cell proliferation process in the ischemically challenged region-at-risk after focal cerebral ischemia in the adult rat brain. A reversible photothrombotic ring stroke model was used, which features sustained hypoperfusion followed by late spontaneous reperfusion and a remarkable morphologic tissue recovery in the anatomically well defined somatosensory cortical region-at-risk. Twelve-week-old male Wistar rats received repeated intraperitoneal injections of the cell proliferation specific marker 5-bromodeoxyuridine (BrdU) after stroke induction. Immunocytochemistry of coronal brain sections revealed that the majority of BrdU-positive cells were of glial, macrophage, and endothelial origin, whereas 3% to 6% of the BrdU-positive cells were double-labeled by BrdU and the neuron-specific marker Map-2 at 7 and 100 days after stroke onset in the region-at-risk. They were distributed randomly in cortical layers II-VI. Three-dimensional confocal analyses of BrdU and the neuronal-specific marker Neu N by double immunofluorescence confirmed their colocalization within the same cells at 72 hours and 30 days after stroke induction. This study suggests that, as a potential pathway for brain repair, new neurons can be generated in the cerebral cortex of adult rats after sublethal focal cerebral ischemia.

scholarly journals Evaluation of the PBR/TSPO Radioligand [18F]DPA-714 in a Rat Model of Focal Cerebral Ischemia

2009 ◽  
Vol 30 (1) ◽  
pp. 230-241 ◽  
Author(s):  
Abraham Martín ◽  
Raphaël Boisgard ◽  
Benoit Thézé ◽  
Nadja Van Camp ◽  
Bertrand Kuhnast ◽  
...  
Keyword(s):  
Cerebral Ischemia ◽  
Pet Imaging ◽  
Time Course ◽  
Focal Cerebral Ischemia ◽  
Quantitative Information ◽  
Translocator Protein ◽  
Experimental Stroke ◽  
Tspo Expression

Focal cerebral ischemia leads to an inflammatory reaction involving an overexpression of the peripheral benzodiazepine receptor (PBR)/18-kDa translocator protein (TSPO) in the cerebral monocytic lineage (microglia and monocyte) and in astrocytes. Imaging of PBR/TSPO by positron emission tomography (PET) using radiolabeled ligands can document inflammatory processes induced by cerebral ischemia. We performed in vivo PET imaging with [18F]DPA-714 to determine the time course of PBR/TSPO expression over several days after induction of cerebral ischemia in rats. In vivo PET imaging showed significant increase in DPA ( N,N-diethyl-2-(2-(4-(2-fluoroethoxy)phenyl)-5,7-dimethylpyrazolo[1,5-a]pyrimidin-3-yl)acetamide) uptake on the injured side compared with that in the contralateral area on days 7, 11, 15, and 21 after ischemia; the maximal binding value was reached 11 days after ischemia. In vitro autoradiography confirmed these in vivo results. In vivo and in vitro [18F]DPA-714 binding was displaced from the lesion by PK11195 and DPA-714. Immunohistochemistry showed increased PBR/TSPO expression, peaking at day 11 in cells expressing microglia/macrophage antigens in the ischemic area. At later times, a centripetal migration of astrocytes toward the lesion was observed, promoting the formation of an astrocytic scar. These results show that [18F]DPA-714 provides accurate quantitative information of the time course of PBR/TSPO expression in experimental stroke.

Loss of cerebral regulation during cardiac output variations in focal cerebral ischemia

1992 ◽  
Vol 77 (2) ◽  
pp. 253-259 ◽  
Author(s):  
Bruce I. Tranmer ◽  
Ted S. Keller ◽  
Glenn W. Kindt ◽  
David Archer
Keyword(s):  
Cardiac Output ◽  
Cerebral Ischemia ◽  
Blood Volume ◽  
Volume Expansion ◽  
Focal Cerebral Ischemia ◽  
Brain Regions ◽  
Ischemic Brain ◽  
Content Type ◽  
Blood Volume Expansion ◽  
Fine Print

✓ Focal cerebral ischemia was induced in anesthetized macaque monkeys by unilateral middle cerebral artery occlusion. The effect of blood volume expansion by a colloid agent and subsequent exsanguination to baseline cardiac output (CO) on local cerebral blood flow (CBF) was measured by the hydrogen clearance technique in both ischemic and nonischemic brain regions. Cardiac output was increased to maximum levels (159% ± 92%, mean ± standard error of the mean) by blood volume expansion with the colloid agent hetastarch, and was then reduced a similar amount (166% ± 82%) by exsanguination during the ischemic period. Local CBF in ischemic brain regions varied directly with CO, with a correlation coefficient of 0.89 (% change CBF/% change CO), while CBF in nonischemic brain was not affected by upward or downward manipulations of CO. The difference in these responses between ischemic and nonischemic brain was highly significant (p < 0.001). The results of this study show a profound loss of regulatory control in ischemic brain in response to alterations in CO, thereby suggesting that blood volume variations may cause significant changes in the intensity of ischemia. It is proposed that CO monitoring and manipulation may be vital for optimum care of patients with acute cerebral ischemia.

Time course of edema formation and brain aquaporin expression after transient focal cerebral ischemia in mice

2005 ◽  
Vol 25 (1_suppl) ◽  
pp. S259-S259 ◽  
Author(s):  
Marlise de Castro Ribeiro ◽  
Lorenz Hirt ◽  
Julien Bogousslavsky ◽  
Luca Regli ◽  
Jerome Badaut
Keyword(s):  
Cerebral Ischemia ◽  
Time Course ◽  
Focal Cerebral Ischemia ◽  
Edema Formation ◽  
Transient Focal Cerebral Ischemia

Time course of aquaporin expression after transient focal cerebral ischemia in mice

2006 ◽  
Vol 83 (7) ◽  
pp. 1231-1240 ◽  
Author(s):  
Marlise de Castro Ribeiro ◽  
Lorenz Hirt ◽  
Julien Bogousslavsky ◽  
Luca Regli ◽  
Jérôme Badaut
Keyword(s):  
Cerebral Ischemia ◽  
Time Course ◽  
Focal Cerebral Ischemia ◽  
Transient Focal Cerebral Ischemia
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