Evaluation of Brain Ischemia in Mice

Ohtaki, Hirokazu; Dohi, Kenji; Nakamachi, Tomoya; Yofu, Sachiko; Endo, S.; Kudo, Yoshifumi; Shioda, Seiji

doi:10.1267/ahc.38.99

Cited by 14 publications

(7 citation statements)

References 59 publications

Supporting

Mentioning

Contrasting

Unclassified

Order By: Relevance

“…The potential for invasion might increase in brain tissue, because craniectomy is also necessary for this method. There are only a small number of reports of the craniectomized model in mice, as the operation is considered technically difficult [23]. On the other hand, the indirect MCAO method occludes the origin of MCA intraluminally with a monofilament thread through the unilateral CCA [3,5,16,27,29,31].…”

Section: Introductionmentioning

confidence: 99%

Direct Experimental Occlusion of the Distal Middle Cerebral Artery Induces High Reproducibility of Brain Ischemia in Mice

et al. 2009

View full text Add to dashboard Cite

Several investigators have used murine models to investigate the pathophysiology of brain ischemia. The focal ischemic model is a closer approximation to human stroke which includes a necrotic core, penumbra, and undamaged tissue. Occlusion of a unilateral artery, especially the middle cerebral artery (MCA), is performed in this model, but collateral circulation often induces variation of ischemic lesions both qualitatively and quantitatively. It is likely that the more proximal the artery which is unilaterally occluded is, the more inconsistent the outcomes. The present study was designed to examine the reproducibility of infarct lesion by distal or proximal artery occlusion. Direct occlusion of the distal MCA was performed and compared with unilateral common carotid artery occlusion (CCAO) in C57BL/6 mice. Direct MCA occlusion (MCAO) consistently induced ischemic lesions in cortical areas. All model animals (n=14) survived 24 h after occlusion, and exhibited a maximum infarct volume (20.0 ± 5.0%). In contrast, permanent and transient unilateral CCAO models had mortality rates of 62.5 and 25.0%, and showed severe to absent lesions with the infarct volumes of 29.0 ± 20.8 and 33.2 ± 24.2%, respectively. In conclusion, distal MCAO produces high reproducibility of ischemic insults and survivability compared to unilateral CCAO. Thus, distal MCAO is a useful method for the focal ischemic model.

show abstract

Section: Introductionmentioning

confidence: 99%

Direct Experimental Occlusion of the Distal Middle Cerebral Artery Induces High Reproducibility of Brain Ischemia in Mice

et al. 2009

View full text Add to dashboard Cite

show abstract

“…BCAO groups were pre-treated with vehicle (saline) or rosiglitizone (5 or 10 mg kg, i.p.) 10 min prior to ischemia * P \ 0.05 relative to BCAO/saline a P \ 0.05 relative to combined controls 1972), and [60% in mice (Ohtaki et al 2005). This blood flow reduction induces partial ischemia, without affecting the circle of Willis, and has been suggested to reflect the early events occurring during transient ischemic attacks (Vanella et al 1992).…”

Section: Discussionmentioning

confidence: 95%

Peroxisome Proliferator-Activated Receptor-γ (PPAR-γ) Activation Confers Functional Neuroprotection in Global Ischemia

Fatehi‐Hassanabad

Tasker

2010

Neurotox Res

View full text Add to dashboard Cite

The neuroprotective effect of rosiglitazone, a peroxisome proliferator-activated receptor γ (PPARγ) agonist, has been investigated using both in vivo and in vitro models of global ischemia in CD1 mice. Behavioral tests were carried out prior to and at various times (up to 14 days) subsequent to bilateral common carotid artery occlusion followed by reperfusion. Mice at each time point were euthanized under anesthesia and the brain was removed, serially sliced and stained with 1% triphenyltetrazolium (TTC) to quantify infarct size. Administration of rosiglitazone (5 or 10 mg/kg, i.p.) 10 min prior to occlusion significantly reduced the postsurgical mortality rate (10-11 vs. 36%, P < 0.05). The higher dose of rosiglitazone (10 mg/kg) also significantly reduced the mean area of brain infarct at 1, 3, 7 and 14 days post-ischemia, reduced post-occlusion deficits in limb grasping and forelimb placing at various time points, and reduced total nitrite concentration in serum and brain homogenate at day 7 post-occlusion. To model global ischemia in vitro, coronal brain slices were incubated in oxygenated artificial cerebrospinal fluid (ACSF) in the presence of either glutamate (1 mM) or hydrogen peroxide (H(2)O(2)) (5 μM) for 30 min. Both H(2)O(2) and glutamate caused significant tissue damage, and co-incubation with rosiglitazone (5 μM) significantly reduced H(2)O(2)-induced damage but did not significantly reduce glutamate-induced brain damage in this model. Our observations provide further evidence for a neuroprotective effect of rosiglitazone in rodent models of ischemia.

show abstract

“…ClC‐3 KO and wild‐type mice were subjected to forebrain ischemia by common carotid artery occlusion (CCAO; Ohtaki et al, 2005, 2008; Inoue et al, 2007). In the first set of experiments, the mice were anesthetized by inhalation of 4.0% sevoflurane, then maintained on 2.5% sevoflurane in N 2 O/O 2 (70/30%) through a facemask.…”

Section: Methodsmentioning

confidence: 99%

Accumulation of autofluorescent storage material in brain is accelerated by ischemia in chloride channel 3 gene‐deficient mice

Ohtaki

Ohara

Song

et al. 2012

J of Neuroscience Research

Self Cite

View full text Add to dashboard Cite

Autofluorescent storage material (ASM) is an aging pigment that accumulates during the normal course of senescence. Although the role of ASM has yet to be fully elucidated, ASM has been implicated in age-related neurodegeneration. In this study, we determined the level of ASM in chloride channel 3 (ClC-3) gene-deficient (KO) mice both in response to aging and following mild global ischemia. To understand the mechanism of action of the ASM, mice subjected to ischemia were treated with the cyclooxygenase (COX) inhibitor indomethacin or with the noncompetitive glutamate receptor antagonist MK-801. ClC-3 KO mice displayed age-related neurodegeneration of the neocortex as well as the hippocampus. The cortical layers in particular granular layers became thinner with aging. ASM accumulated in the brains of ClC-3 KO mice was increased seven- to 50-fold over that observed in the corresponding regions of their wild-type littermates. Young wild-type mice survived longer than age-matched ClC-3 KO mice after permanent global ischemia. However, in the case of older animals, the survival curves were similar. The ASM also increased four- to fivefold 10 days after mild global ischemia, an effect that was suppressed by treatment with indomethacin and MK-801. These results suggest that temporary ischemia might trigger a process similar to aging in the brain, mimicking the effect of age-related neurodegenerative diseases.

show abstract

Evaluation of Brain Ischemia in Mice

Cited by 14 publications

References 59 publications

Direct Experimental Occlusion of the Distal Middle Cerebral Artery Induces High Reproducibility of Brain Ischemia in Mice

Direct Experimental Occlusion of the Distal Middle Cerebral Artery Induces High Reproducibility of Brain Ischemia in Mice

Peroxisome Proliferator-Activated Receptor-γ (PPAR-γ) Activation Confers Functional Neuroprotection in Global Ischemia

Accumulation of autofluorescent storage material in brain is accelerated by ischemia in chloride channel 3 gene‐deficient mice

Contact Info

Product

Resources

About