Evaluation of MCAO stroke models in normotensive rats: standardized neocortical infarction by the 3VO technique

Yanamoto, Hiroji; Nagata, Izumi; Niitsu, Yasushi; Xue, Jing; Zhang, Zhiwen; Kikuchi, Hiroe

doi:10.1016/s0014-4886(03)00116-x

Cited by 60 publications

(50 citation statements)

References 76 publications

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“…[91][92][93][94] In the rat, variations on the three-vessel occlusion model relate to whether the MCA and ipsilateral carotid arteries are permanently or transiently occluded. These variations include permanent occlusion of the ipsilateral common and middle cerebral carotid arteries, 92 permanent occlusion of the ipsilateral common carotid artery alone, 95 permanent occlusion of the middle cerebral artery alone, 94 and temporary occlusion of all three vessels. 96 A comparison of infarct size across these variations suggests that this approach generates a reproducible infarct volume, especially within the same lab.…”

Section: Other Models Of Mcao: Distal Mcao and Embolic Mcaomentioning

confidence: 99%

“…128 To define the cellular and molecular mechanisms of these reparative processes requires that an animal model allow direct study of the relevant neuronal circuits as they sprout, differentiate, or re-map after stroke. Most of the animal models of cell death in stroke, including suture occlusion of the MCA, the Tamura model, embolic MCAo and the three-vessel model, produce substantial damage to many different brain regions, sparing very rostral and medial frontal cortex, lateral temporal cortex and occipital cortex 89,92,95,129 (FIG. 1).…”

Section: Animal Models Of Neural Repair In Strokementioning

confidence: 99%

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Rodent models of focal stroke: Size, mechanism, and purpose

2005

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Summary: Rodent stroke models provide the experimental backbone for the in vivo determination of the mechanisms of cell death and neural repair, and for the initial testing of neuroprotective compounds. Less than 10 rodent models of focal stroke are routinely used in experimental study. These vary widely in their ability to model the human disease, and in their application to the study of cell death or neural repair. Many rodent focal stroke models produce large infarcts that more closely resemble malignant and fatal human infarction than the average sized human stroke. This review focuses on the mechanisms of ischemic damage in rat and mouse stroke models, the relative size of stroke generated in each model, and the purpose with which focal stroke models are applied to the study of ischemic cell death and to neural repair after stroke.

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Section: Other Models Of Mcao: Distal Mcao and Embolic Mcaomentioning

confidence: 99%

Section: Animal Models Of Neural Repair In Strokementioning

confidence: 99%

Rodent models of focal stroke: Size, mechanism, and purpose

2005

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“…Model-Temporary focal ischemia was induced using the three-vessel occlusion technique as described previously (34). Briefly, under halothane-inhalation anesthesia, the left middle cerebral artery of each mouse (8 -19 weeks old) was cauterized at the lateral border of the olfactory tract, and bilateral common carotid arteries were clip-occluded for 15 min followed by reperfusion.…”

Section: Middle Cerebral Artery Occlusion (Mcao)mentioning

confidence: 99%

“…Regional Cerebral Blood Flow (rCBF) in the Penumbra-like Peripheral Area-The rCBF was monitored using the laserDoppler blood flowmetry meter TBF-LN1 (Unique Medical) (34). The measurement area was set in the penumbra-like peripheral area of the ischemic region at 2 mm caudal and 1 mm dorsal to the crossover point of the left middle cerebral artery and the lateral surface of the olfactory tract.…”

Section: Middle Cerebral Artery Occlusion (Mcao)mentioning

confidence: 99%

NDRG4 Protein-deficient Mice Exhibit Spatial Learning Deficits and Vulnerabilities to Cerebral Ischemia

Yamamoto

Kokame

Okuda

et al. 2011

Journal of Biological Chemistry

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The N-myc downstream-regulated gene (NDRG) family consists of four related proteins, NDRG1-NDRG4, in mammals. We previously generated NDRG1-deficient mice that were unable to maintain myelin sheaths in peripheral nerves. This condition was consistent with human hereditary motor and sensory neuropathy, Charcot-Marie-Tooth disease type 4D, caused by a nonsense mutation of NDRG1. In contrast, the effects of genetic defects of the other NDRG members remain unknown. In this study, we focused on NDRG4, which is specifically expressed in the brain and heart. In situ mRNA hybridization on the brain revealed that NDRG4 was expressed in neurons of various areas. We generated NDRG4-deficient mice that were born normally with the expected Mendelian frequency. Immunochemical analysis demonstrated that the cortex of the NDRG4-deficient mice contained decreased levels of brain-derived neurotrophic factor (BDNF) and normal levels of glial cell line-derived neurotrophic factor, NGF, neurotrophin-3, and TGF-␤1. Consistent with BDNF reduction, NDRG4-deficient mice had impaired spatial learning and memory but normal motor function in the Morris water maze test. When temporary focal ischemia of the brain was induced, the sizes of the infarct lesions were larger, and the neurological deficits were more severe in NDRG4-deficient mice compared with the control mice. These findings indicate that NDRG4 contributes to the maintenance of intracerebral BDNF levels within the normal range, which is necessary for the preservation of spatial learning and the resistance to neuronal cell death caused by ischemic stress. N-myc downstream-regulated gene (NDRG)3 family members NDRG1-NDRG4 are intracellular proteins, consist of 340 -394 amino acid residues, and share 53-65% sequence identity with each other. Furthermore, accumulating evidence implicates their roles in development, cancer metastasis, and the immune system (1-5).We originally identified RTP (NDRG1) as a homocysteineresponsive gene in human umbilical vein endothelial cells (6), which is also called DRG1, Cap43, Rit42, Ndr1, and PROXY-1. NDRG1 expression is induced by a number of conditions, such as DNA damage, hypoxia, and intracellular calcium ion elevation (4). Overexpression of NDRG1 suppresses the metastatic potency of some types of cancer cells (4) and enhances the degranulation of mast cells in response to various stimuli (7). A nonsense mutation of NDRG1 causes hereditary motor and sensory neuropathy, Charcot-Marie-Tooth disease type 4D, which presents as distal muscle wasting and atrophy, foot and hand deformities, tendon areflexia, sensory loss, and deafness in afflicted individuals (8). We previously generated NDRG1-deficient mice and revealed the essential role of NDRG1 in the cytoplasm of Schwann cells for the maintenance of myelin sheaths in peripheral nerves (9). A frame shift deletion of Ndrg1 in Greyhounds also causes polyneuropathy (10).Similar to NDRG1, the expression of NDRG2 is induced by stress conditions such as hypoxia (1). NDRG2 expression is upregulated in cort...

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“…The mouse model of middle cerebral artery occlusion has been described by Connolly et al (1996) and has also been been modified and used by several researchers (Olsen et al, 1986;Clark et al, 1997;Belayev et al, 1999). Various anesthetic gases have also been used for the mouse model of middle cerebral artery occlusion (Yanamoto et al, 2003) with no correlation on the effect of the choice of anesthetic to the engraftment potential of the HSC. The duration of occluison also varies from 45 minutes to 120 minutes (Campagne et al, 1999).…”

Section: Are Hsc a Viable Avenue For Stroke Therapy?mentioning

confidence: 99%