Cumulative white matter changes in the gerbil brain under chronic cerebral hypoperfusion

Hattori, Hideyuki; Takeda, Masatoshi; Kudo, Takashi; Nishimura, Tsunehiko; Hashimoto, Shigeo

doi:10.1007/bf00227672

Cited by 57 publications

(34 citation statements)

References 11 publications

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“…Following chronic hypoperfusion, animals developed learning impairments in a passive avoidance paradigm (Kudo et al, 1990). Lesions specific to WM, resembling the leukoariosis seen in the aging brain, were also seen in these animals (Hattori et al, 1992). Western blotting was used to examine the molecular changes in WM following chronic hypoperfusion.…”

Section: Discussionmentioning

confidence: 99%

Brain macrostructural and microstructural abnormalities in cocaine dependence

Lim

Wozniak

Mueller

et al. 2008

Drug and Alcohol Dependence

144

115

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Rationale-Two previous studies have utilized Diffusion Tensor Imaging (DTI) to examine microstructural integrity in cocaine abuse and found evidence of brain abnormalities in white matter.Objective-Using anatomical magnetic resonance imaging (MRI), DTI, and clinical evaluation, the macrostructural and microstructural correlates of cocaine abuse were investigated.Methods-21 men and women (mean age 42.5, mean 18.9 years of cocaine use) and 21 age/gendermatched controls were included. Fractional anisotropy (FA) was measured in frontal white matter ROIs. Gray and white matter volumes in superior and inferior frontal regions were compared.Results-DTI data revealed that cocaine users had lower FA than controls, specifically in inferior frontal white matter. FA differences were not seen in other areas. Significant volumetric differences were not seen, but both grey and white matter inferior frontal volumes trended toward smaller in the cocaine group. The data suggested that duration of use was associated with decreased grey and white matter volumes. FA and grey matter volume were correlated in cocaine users.Conclusions-Both macrostructural and microstructural abnormalities were seen in a group of cocaine abusers. Length of cocaine use was associated with severity of the brain abnormalities. Future studies of white matter tissue integrity are warranted including examination of the relationship between DTI measures and traditional volumetric measures.

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Section: Discussionmentioning

confidence: 99%

Brain macrostructural and microstructural abnormalities in cocaine dependence

Lim

Wozniak

Mueller

et al. 2008

Drug and Alcohol Dependence

144

115

View full text Add to dashboard Cite

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“…1 In support for this hypothesis, hypoxia-inducible factor-1 is expressed in cerebrovascular WM lesions. 2 In addition, WM lesions are observed in rodent models of chronic cerebral hypoperfusion, in which the bilateral carotid arteries are stenosed or ligated, [3][4][5][6][7] and stroke-prone spontaneously hypertensive rats which have small vessel pathology. 8 Such WM lesions are suggested to contribute to frontal hypometabolism and executive dysfunction.…”

mentioning

confidence: 99%

Selective Impairment of Working Memory in a Mouse Model of Chronic Cerebral Hypoperfusion

Shibata

Yamasaki²,

Miyakawa³

et al. 2007

Stroke

219

225

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Background and Purpose-We recently designed a mouse model of chronic cerebral hypoperfusion, in which the cerebral white matter is damaged without significant gray matter lesions. The behavioral characteristics of these mice were studied using a test battery for neurological and cognitive functions. Methods-Adult C57Bl/6 male mice were subjected to either sham-operation or bilateral common carotid artery stenosis (BCAS) using microcoils with an internal diameter of 0.18 mm. At 30 days after BCAS, 70 animals were divided into 3 groups and subjected to behavioral test batteries. The first group underwent comprehensive behavioral test, including the neurological screen, prepulse inhibition, hot plate, open field, light/dark transition, Porsolt forced swim and contextual and cued fear conditioning (BCAS nϭ13; sham-operated nϭ11). The second group was for the working memory task of the 8-arm radial maze test (BCAS nϭ12; sham-operated nϭ10), and the third for the reference memory task of the 8-arm radial maze test (BCAS nϭ13; sham-operated nϭ11). Another batch of animals were examined for histological changes (BCAS nϭ11; sham-operated nϭ12). Results-The white matter including the corpus callosum was consistently found to be rarefied without clear ischemic lesions in the hippocampus. No apparent differences were observed in the comprehensive test batteries between the control and BCAS mice. However, in the working memory tasks tested with the 8-arm radial maze, the BCAS mice made significantly more errors than the control mice (PϽ0.0001). Again, there were no detectable differences in the reference memory tasks between the groups. Conclusions-At 30 days after BCAS, working memory deficits as well as white matter changes were apparent in the mice.Working memory deficit was attributable to damage of the frontal-subcortical circuits, suggesting the BCAS model is useful to evaluate the substrates of subcortical vascular dementia.

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“…The regional blood flow is restored by 3 h. Interestingly, ischemia induced by ET-1 administration does not appear to affect BBB integrity. Contrast-enhanced T1-weighted images show that Hattori et al [43] and Kudo et al [44] 1992 and 1993 Gerbil…”

Section: Et-1/vasoconstriction Methodsmentioning

confidence: 99%

“…Bilateral common carotid stenosis has been reported in both gerbil (with an incomplete circle of Willis) [43][44][45] and mouse [46,47]. The stenosis is produced by placing a surgical coil around the common carotid arteries bilaterally, which incompletely obstructs the vessel and produces~25% reduction in cerebral blood flow in both species [44,46].…”

Section: Carotid Occlusion/stenosis Modelsmentioning

confidence: 99%

“…The stenosis is produced by placing a surgical coil around the common carotid arteries bilaterally, which incompletely obstructs the vessel and produces~25% reduction in cerebral blood flow in both species [44,46]. In the gerbil, this produces necrotic foci in both gray and white matter structures with dendritic swelling and myelin loss [43], predominantly in a pattern of watershed ischemia [44]. The lesions develop more slowly at >8 weeks and are associated with learning impairment [44].…”

Section: Carotid Occlusion/stenosis Modelsmentioning

confidence: 99%

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Models That Matter: White Matter Stroke Models

2012

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Summary Stroke is a devastating neurological disease with limited functional recovery. Stroke affects all cellular elements of the brain and impacts areas traditionally classified as both gray matter and white matter. In fact, stroke in subcortical white matter regions of the brain accounts for approximately 30% of all stroke subtypes, and white matter injury is a component of most classes of stroke damage. However, most basic scientific information in stroke cell death and neural repair relates principally to neuronal cell death and repair. Despite an emerging biological understanding of white matter development, adult function, and reorganization in inflammatory diseases, such as multiple sclerosis, little is known of the specific molecular and cellular events in white matter ischemia. This limitation stems in part from the difficulty in generating animal models of white matter stroke. This review will discuss recent progress in studies of animal models of white matter stroke, and the emerging principles of cell death and repair in oligodendrocytes, axons, and astrocytes in white matter ischemic injury.Key Words Ischemia . oligodendrocyte . oligodendrocyte progenitor cell . mouse . rat . axoglial unit . endothelin Clinical Aspects of White Matter StrokeSubcortical white matter stroke constitutes 15 to 25% of all stroke subtypes [1,2]. These lesions encompass small infarcts in deep penetrating vessels in the brain [3][4][5]. In traditional stroke subtyping, subcortical or white matter stroke includes infarcts in the white matter deep to the cortex in humans, and also small basal ganglia, thalamus, and brainstem strokes or "lacunar" infarctions. Recent studies indicate distinct clinicopathological entities between subcortical white matter versus brainstem, thalamic, or basal ganglia lacunar infarctions. Subcortical white matter infarctions are more closely related to microvascular stroke risk factors, such as hypertension and diabetes, and appear to involve a spectrum, especially as seen in magnetic resonance imaging (MRI), of ischemic white matter hyperintensities to small necrotic cavities [4]. Pathologically, white matter strokes progress and enlarge: repeat MRI imaging shows that new white matter strokes develop within pre-existing lesions and also are associated with adjacent lesions in 71% of cases [4]. Interestingly, this tissue progression from recent MRI studies resembles the original description of the pathology of lacunar infarcts from Dechambre in 1838 of a central lesion of "softening," which is then absorbed to produce the necrotic cavity [6]. This current and historical perspective indicates that the specific ischemic focus in white matter is distinct from that of large vessel disease, and is a progressive focal lesion.Subcortical white matter stroke has devastating clinical consequences. This was first cohesively presented by Pierre Marie, who described the accumulation of small clinical strokes into a progressive state, an état lacunaire, of motor slowing and global intellectual deterioration [7...

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Cumulative white matter changes in the gerbil brain under chronic cerebral hypoperfusion

Cited by 57 publications

References 11 publications

Brain macrostructural and microstructural abnormalities in cocaine dependence

Brain macrostructural and microstructural abnormalities in cocaine dependence

Selective Impairment of Working Memory in a Mouse Model of Chronic Cerebral Hypoperfusion

Models That Matter: White Matter Stroke Models

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