A photothrombotic model of small early ischemic infarcts in the rat brain with histologic and MRI correlation

Pevsner, Paul H.; Eichenbaum, Joseph W.; Miller, Douglas C.; Pivawer, Gabriel; Eichenbaum, Kenneth D.; Stern, Arnold; Zakian, Kristin L.; Koutcher, Jason A.

doi:10.1016/s1056-8719(01)00153-8

Cited by 60 publications

(43 citation statements)

References 10 publications

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“…Unilateral focal photothrombotic infarction in the rat primary somatosensory cortex was induced according to [18,19]. The rats were anesthetized with chloral hydrate (300 mg/kg, i.p.).…”

Section: Focal Photothrombotic Ischemia In the Rat Cerebral Cortexmentioning

confidence: 99%

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Protein Profile and Morphological Alterations in Penumbra after Focal Photothrombotic Infarction in the Rat Cerebral Cortex

et al. 2016

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After ischemic stroke, cell damage propagates from infarct core to surrounding tissues (penumbra). To reveal proteins involved in neurodegeneration and neuroprotection in penumbra, we studied protein expression changes in 2-mm ring around the core of photothrombotic infarct induced in the rat brain cortex by local laser irradiation after administration of Bengal Rose. The ultrastructural study showed edema and degeneration of neurons, glia, and capillaries. Morphological changes gradually decreased across the penumbra. Using the antibody microarrays, we studied changes in expression of >200 neuronal proteins in penumbra 4 or 24 h after focal photothrombotic infarct. Diverse cellular subsystems were involved in the penumbra tissue response: signal transduction pathways such as protein kinase Bα/GSK-3, protein kinase C and its β1 and β2 isoforms, Wnt/β-catenin (axin1, GSK-3, FRAT1), Notch/NUMB, DYRK1A, TDP43; mitochondria quality control (Pink1, parkin, HtrA2); ubiquitin-mediated proteolysis (ubiquilin-1, UCHL1); axon outgrowth and guidance (NAV-3, CRMP2, PKCβ2); vesicular trafficking (syntaxin-8, TMP21, Munc-18-3, synip, ALS2, VILIP1, syntaxin, synaptophysin, synaptotagmin); biosynthesis of neuromediators (tryptophan hydroxylase, monoamine oxidase B, glutamate decarboxylase, tyrosine hydroxylase, DOPA decarboxylase, dopamine transporter); intercellular interactions (N-cadherin, PMP22); cytoskeleton (neurofilament 68, neurofilament-M, doublecortin); and other proteins (LRP1, prion protein, β-amyloid). These proteins are involved in neurodegeneration or neuroprotection. Such changes were most expressed 4 h after photothrombotic impact. Immunohistochemical and Western blot studies of expression of monoamine oxidase B, UCHL1, DYRK1A, and Munc-18-3 confirmed the proteomic data. These data provide the integral view on the penumbra response to photothrombotic infarct. Some of these proteins can be potential targets for ischemic stroke therapy.

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“…Unilateral focal photothrombotic infarction in the rat primary somatosensory cortex was induced according to [18,19]. The rats were anesthetized with chloral hydrate (300 mg/kg, i.p.).…”

Section: Focal Photothrombotic Ischemia In the Rat Cerebral Cortexmentioning

confidence: 99%

“…The following local photoirradiation induces focal oxidative damage of the vascular endothelium, platelet aggregation, and occlusion of microvessels. This PTI model is slightlyinvasive.Theinjurylocation,size,anddegreearewellcontrolled and reproducible [15][16][17][18]. However, penumbra resulting from such impact is rather narrow.…”

Section: Introductionmentioning

confidence: 99%

Protein Profile and Morphological Alterations in Penumbra after Focal Photothrombotic Infarction in the Rat Cerebral Cortex

et al. 2016

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“…Small cortical infarcts, produced in rats by occluding a cortical pial artery on the brain surface using forceps or photochemical irradiation, 43,45 were described as mimicking lacunar infarction because they showed "cavitation caused specifically by ischemia of smaller vessels" (however, the lesions were cortical). 41 In primates, a balloon cuff placed around the proximal middle cerebral artery to occlude the lenticulostriate arteries 40 leaving the middle cerebral artery patent, resulted in lenticulostriate artery occlusion by eosinophilic thrombus with brain tissue softening, necrosis, and cyst formation of 3.9 cm 3 average volume.…”

Section: Perforating Artery Occlusionmentioning

confidence: 99%

Potential Animal Models of Lacunar Stroke

Bailey

McCulloch

Sudlow

et al. 2009

Stroke

116

108

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Background and Purpose-Lacunar ischemic stroke accounts for 25% of all ischemic strokes, but the exact etiology is unknown. Numerous pathophysiologies have been proposed, including atheroma and endothelial dysfunction. Models of any of these pathological features would aid understanding of the etiology and help develop treatments for lacunar stroke. We therefore aimed to assess the relevance of all available potential animal models of lacunar stroke. Methods-We systematically reviewed the published literature for animal models that could represent lacunar stroke using validated search strategies. We included studies that could represent an aspect of lacunar stroke as well as those aiming to model conditions with potentially similar pathology and extracted data on species, induction method, and resulting brain and vessel lesions. Results-From 5670 papers, 41 studies (46 papers) met inclusion criteria representing over 10 different classes of stroke induction. Important data like infarct size and animal numbers were often missing. Many models' infarcts were too large or affected the cortex. Emboli mostly caused cortical but not small subcortical lesions. Most models focused on creating ischemic lesions in brain tissue. Only one (spontaneous lesions in spontaneously hypertensive stroke-prone rats) also mimicked small vessel pathology. Here, the precursor to small vessel and brain damage was blood-brain barrier failure. Conclusion-Some animal models produce small subcortical infarcts, but few mimic the human small vessel pathology.Models of small vessel disease could help improve understanding of human lacunar disease, particularly to clarify factors associated with the small vessel morphological changes preceding brain damage. Much lacunar stroke may arise after blood-brain barrier disruption. (Stroke. 2009;40:e451-e458.)

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“…They are easily controlled by the irradiation intensity and duration, beam position, and dye concentration. [45][46][47][48] PTI is characterized by a low animal mortality (<10%) and prolonged sensorimotor impairment. [49][50][51] The 2-laser system, in which Bengal Rose-mediated photothrombosis was induced by 568-nm krypton laser irradiation and 355-nm UV light of YAG laser induced reperfusion, provides a less invasive and reproducible focal ischemia.…”

Section: Photothrombotic Strokementioning

confidence: 99%

Photodynamic therapy: a review of applications in neurooncology and neuropathology

et al. 2015

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A photothrombotic model of small early ischemic infarcts in the rat brain with histologic and MRI correlation

Cited by 60 publications

References 10 publications

Protein Profile and Morphological Alterations in Penumbra after Focal Photothrombotic Infarction in the Rat Cerebral Cortex

Protein Profile and Morphological Alterations in Penumbra after Focal Photothrombotic Infarction in the Rat Cerebral Cortex

Potential Animal Models of Lacunar Stroke

Photodynamic therapy: a review of applications in neurooncology and neuropathology

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