An objective procedure for ischemic area evaluation of the stroke intraluminal thread model in the mouse and rat

Wexler, Eric J.; Peters, Elaine E.; Gonzales, Armando; Gonzales, Maria; Slee, Andrew M.; Kerr, Janet S.

doi:10.1016/s0165-0270(01)00476-9

Cited by 51 publications

(46 citation statements)

References 21 publications

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“…On the other hand, the thread MCAO model has a different CIV peak. The thread-permanent MCAO induces peak CIV at 18 h in C57BL/6 mice, and at 24 h in rats [31]. The difference in CIV peak time would be explained by differences of angioarchitectural anastomoses or speed of autolysis among rodent species [15,26,34].…”

Section: Discussionmentioning

confidence: 98%

“…Established intraluminal thread methods [3,5,12,16,29,31] occlude the ICA at the origin of the MCA (Fig. 1A), whereas the direct MCAO occludes a more distal portion of the MCA (Fig.…”

Section: Surgical Preparation and Direct Mcaomentioning

confidence: 99%

“…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]. The intraluminal thread model has the benefit of no brain invasion, so that a large number of studies can be performed under these conditions.…”

Section: Introductionmentioning

confidence: 99%

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

et al. 2009

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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.

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Section: Discussionmentioning

confidence: 98%

“…Established intraluminal thread methods [3,5,12,16,29,31] occlude the ICA at the origin of the MCA (Fig. 1A), whereas the direct MCAO occludes a more distal portion of the MCA (Fig.…”

Section: Surgical Preparation and Direct Mcaomentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

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

et al. 2009

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“…in 2% 2, 3, 5‐triphenyltetrazolium chloride (TTC) (Sigma‐Aldrich, St. Louise, MO 63103, USA) solution at 37°C and then scanned into the computer. The photographs were analysed using Image Pro Plus 6.0 (Media Cybernetics, Silver Spring, MD, USA) according to previous report 31. The cerebral oedema rate is given by the equation:

(S) = (\sum LT - \sum RT) / (\sum LT + \sum RT) \times 100 %

where ΣLT and ΣRT represent the volume of left (ischaemic) and right (non‐ischaemic) hemisphere, respectively.…”

Section: Methodsmentioning

confidence: 99%

cPKCγ‐mediated down‐regulation ofUCHL1 alleviates ischaemic neuronal injuries by decreasing autophagyviaERK‐mTORpathway

Zhang

Han

Wang

et al. 2017

J Cellular Molecular Medi

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Stroke is one of the leading causes of death in the world, but its underlying mechanisms remain unclear. Both conventional protein kinase C (cPKC)γ and ubiquitin C‐terminal hydrolase L1 (UCHL1) are neuron‐specific proteins. In the models of 1‐hr middle cerebral artery occlusion (MCAO)/24‐hr reperfusion in mice and 1‐hr oxygen–glucose deprivation (OGD)/24‐hr reoxygenation in cortical neurons, we found that cPKCγ gene knockout remarkably aggravated ischaemic injuries and simultaneously increased the levels of cleaved (Cl)‐caspase‐3 and LC3‐I proteolysis product LC3‐II, and the ratio of TUNEL‐positive cells to total neurons. Moreover, cPKCγ gene knockout could increase UCHL1 protein expression via elevating its mRNA level regulated by the nuclear factor κB inhibitor alpha (IκB‐α)/nuclear factor κB (NF‐κB) pathway in cortical neurons. Both inhibitor and shRNA of UCHL1 significantly reduced the ratio of LC3‐II/total LC3, which contributed to neuronal survival after ischaemic stroke, but did not alter the level of Cl‐caspase‐3. In addition, UCHL1 shRNA reversed the effect of cPKCγ on the phosphorylation levels of mTOR and ERK rather than that of AMPK and GSK‐3β. In conclusion, our results suggest that cPKCγ activation alleviates ischaemic injuries of mice and cortical neurons through inhibiting UCHL1 expression, which may negatively regulate autophagy through ERK‐mTOR pathway.

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“…Brain sections were incubated for 20 min in a solution of 0.5% 2,3,5-triphenyltetrazolium chloride (TTC) in 0.01 M PBS at 37°C, and then the slices were photographed by a scanner. These images were analyzed using Image Pro Plus 6.0 (Media Cybernetics) according to Eric's ischemic area evaluation procedure (Wexler et al, 2002). Edema was calculated using the equation: E ϭ (ΑVL Ϫ ΑVR)/(ΑVL ϩ ΑVR)*100%, where ΑVL and ΑVR are the volume of left and right hemisphere volume, respectively.…”

Section: Methodsmentioning

confidence: 99%

The DREAM Protein Negatively Regulates the NMDA Receptor through Interaction with the NR1 Subunit

Zhang

Liang

et al. 2010

J. Neurosci.

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Glutamate-induced excitotoxicity has been implicated in the etiology of stroke, epilepsy, and neurodegenerative diseases. NMDA receptors (NMDARs) play a pivotal role in excitotoxic injury; however, clinical trials testing NMDAR antagonists as neuroprotectants have been discouraging. The development of novel neuroprotectant molecules is being vigorously pursued. Here, we report that downstream regulatory element antagonist modulator (DREAM) significantly inhibits surface expression of NMDARs and NMDAR-mediated current. Overexpression of DREAM showed neuroprotection against excitotoxic neuronal injury, whereas knockdown of DREAM enhanced NMDA-induced toxicity. DREAM could directly bind to the C0 domain of the NR1 subunit. Although DREAM contains multiple binding sites for the NR1 subunit, residues 21-40 of the N terminus are the main binding site for the NR1 subunit. Thus, 21-40 residues might relieve the autoinhibition conferred by residues 1-50 and derepress the DREAM core domain by a competitive mechanism. Intriguingly, the cell-permeable TAT-21-40 peptide, constructed according to the critical binding site of DREAM to the NR1 subunit, inhibits NMDARmediated currents in primary cultured hippocampal neurons and has a neuroprotective effect on in vitro neuronal excitotoxic injury and in vivo ischemic brain damage. Moreover, both pretreatment and posttreatment of TAT-21-40 is effective against excitotoxicity. In summary, this work reveals a novel, negative regulator of NMDARs and provides an attractive candidate for the treatment of excitotoxicity-related disease.

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An objective procedure for ischemic area evaluation of the stroke intraluminal thread model in the mouse and rat

Cited by 51 publications

References 21 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

cPKCγ‐mediated down‐regulation ofUCHL1 alleviates ischaemic neuronal injuries by decreasing autophagyviaERK‐mTORpathway

The DREAM Protein Negatively Regulates the NMDA Receptor through Interaction with the NR1 Subunit

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