Evaluation of Survival and Neurological Deficit in Rats in the New Model of Global Transient Cerebral Ischemia

Чернышева, Г. А.; Smol’yakova, V. I.; Osipenko, Anton N.; Mb, Plotnikov

doi:10.1007/s10517-014-2721-8

Cited by 7 publications

(6 citation statements)

References 10 publications

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“…The surgery was performed as described previously [ 16 , 72 ]. Briefly, rats were anesthetized with chloral hydrate in a dose of 450 mg/kg intraperitoneally (Sigma-Aldrich Chemical Co., St. Louis, MO, USA) and placed on a homeothermic blanket (Temperature Control Unit HB 101/2, Letica Scientific Instruments, Barcelona, Spain) in a supine position.…”

Section: Methodsmentioning

confidence: 99%

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Neurodegeneration, Myelin Loss and Glial Response in the Three-Vessel Global Ischemia Model in Rat

Ананьина

Kisel

Kudabaeva

et al. 2020

IJMS

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(1) Background: Although myelin disruption is an integral part of ischemic brain injury, it is rarely the subject of research, particularly in animal models. This study assessed for the first time, myelin and oligodendrocyte loss in a three-vessel model of global cerebral ischemia (GCI), which causes hippocampal damage. In addition, we investigated the relationships between demyelination and changes in microglia and astrocytes, as well as oligodendrogenesis in the hippocampus; (2) Methods: Adult male Wistar rats (n = 15) underwent complete interruption of cerebral blood flow for 7 min by ligation of the major arteries supplying the brain or sham-operation. At 10 and 30 days after the surgery, brain slices were stained for neurodegeneration with Fluoro-Jade C and immunohistochemically to assess myelin content (MBP+ percentage of total area), oligodendrocyte (CNP+ cells) and neuronal (NeuN+ cells) loss, neuroinflammation (Iba1+ cells), astrogliosis (GFAP+ cells) and oligodendrogenesis (NG2+ cells); (3) Results: 10 days after GCI significant myelin and oligodendrocyte loss was found only in the stratum oriens and stratum pyramidale. By the 30th day, demyelination in these hippocampal layers intensified and affected the substratum radiatum. In addition to myelin damage, activation and an increase in the number of microglia and astrocytes in the corresponding layers, a loss of the CA1 pyramidal neurons, and neurodegeneration in the neocortex and thalamus was observed. At a 10-day time point, we observed rod-shaped microglia in the substratum radiatum. Parallel with ongoing myelin loss on the 30th day after ischemia, we found significant oligodendrogenesis in demyelinated hippocampal layers; (4) Conclusions: Our study showed that GCI-simulating cardiac arrest in humans—causes not only the loss of pyramidal neurons in the CA1 field, but also the myelin loss of adjacent layers of the hippocampus.

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Section: Methodsmentioning

confidence: 99%

“…At Days 11 and 31 after surgery, neurological deficit was evaluated with the Stroke-index McGraw scale [ 72 , 73 ].…”

Section: Methodsmentioning

confidence: 99%

Neurodegeneration, Myelin Loss and Glial Response in the Three-Vessel Global Ischemia Model in Rat

Ананьина

Kisel

Kudabaeva

et al. 2020

IJMS

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“…Acute global cerebral ischemia was induced according to the new 3-vessel model, as detailed elsewhere [ 30 , 31 ]. Briefly, rats were anesthetized with chloral hydrate in a dose of 450 mg/kg intraperitoneally (Sigma-Aldrich Chemical Co., St. Louis, MO, USA) and placed on a homeothermic blanket (Temperature Control Unit HB 101/2, Letica Scientific Instruments, Barcelona, Spain) in a supine position.…”

Section: Methodsmentioning

confidence: 99%

“…The studies performed on the two-vessel GCI model in gerbils [ 28 ] and mice [ 27 ] have shown neuroprotective effect of fluoxetine in the hippocampus. Preliminary results of our study [ 10 ] based on the rat three-vessel occlusion GCI model [ 30 , 31 ] have shown a decrease in the number of immature neurons in the DG after fluoxetine treatment at later observation times (30 days). Clearly, these limited observations do not provide a complete picture of a potential therapeutic effect of fluoxetine in GCI and warrant further studies.…”

Section: Introductionmentioning

confidence: 92%

“…Such a condition occurs if the brain completely loses blood supply, and it is clinically related to the transient cardiac arrest. Several GCI models have been developed including the two-vascular model of forebrain ischemia in gerbils [ 14 , 16 , 24 ], the two-vascular cerebral ischemia model in rats with hypotension [ 15 ], murine chemically-induced cardiac arrest model [ 29 ], and a recent three-vessel rat occlusion model [ 30 , 31 ]. As compared to focal ischemic infarct models, GCI models are less standardized and used less frequently.…”

Section: Introductionmentioning

confidence: 99%

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Effects of Fluoxetine on Hippocampal Neurogenesis and Neuroprotection in the Model of Global Cerebral Ischemia in Rats

Khodanovich

Kisel

Kudabaeva

et al. 2018

IJMS

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A selective serotonin reuptake inhibitor, fluoxetine, has recently attracted a significant interest as a neuroprotective therapeutic agent. There is substantial evidence of improved neurogenesis under fluoxetine treatment of brain ischemia in animal stroke models. We studied long-term effects of fluoxetine treatment on hippocampal neurogenesis, neuronal loss, inflammation, and functional recovery in a new model of global cerebral ischemia (GCI). Brain ischemia was induced in adult Wistar male rats by transient occlusion of three main vessels originating from the aortic arch and providing brain blood supply. Fluoxetine was injected intraperitoneally in a dose of 20 mg/kg for 10 days after surgery. To evaluate hippocampal neurogenesis at time points 10 and 30 days, 5-Bromo-2′-deoxyuridine was injected at days 8–10 after GCI. According to our results, 10-day fluoxetine injections decreased neuronal loss and inflammation, improved survival and functional recovery of animals, enhanced neurogenesis, and prevented an early pathological increase in neural stem cell recruitment in the subgranular zone (SGZ) of the hippocampus without reducing the number of mature neurons at day 30 after GCI. In summary, this study suggests that fluoxetine may provide a promising therapy in cerebral ischemia due to its neuroprotective, anti-inflammatory, and neurorestorative effect.

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Effect of Fluoxetine on Neurogenesis in Hippocampal Dentate Gyrus after Global Transient Cerebral Ischemia in Rats

et al. 2016

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Changes in cerebral neurogenesis provoked by ischemia and the effect of fluoxetine on this process were studied using a three-vessel occlusion model of global transient cerebral ischemia. The global transient cerebral ischemia was modeled on male Wistar rats by transient occlusion of three major vessels originating from the aortic arch and supplying the brain (brachiocephalic trunk, left subclavian artery, and left common carotid artery). The cells expressing doublecortin (DCX, a marker of young neurons) were counted in the hippocampal dentate gyrus on day 31 after ischemia modeling. It was found that ischemia inhibited neurogenesis in the dentate gyrus in comparison with sham-operated controls (p<0.05), while fluoxetine (20 mg/kg/day) injected over 10 days after surgery restored neurogenesis to the control level (p<0.001).

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Evaluation of Survival and Neurological Deficit in Rats in the New Model of Global Transient Cerebral Ischemia

Abstract: We propose a modification to rat model of transient global cerebral ischemia with four-vessel occlusion avoiding pneumothorax and minimizing the consequences of surgery. Survival and neurological deficit in rats in this model was studied over 5 days.

Cited by 7 publications

References 10 publications

Neurodegeneration, Myelin Loss and Glial Response in the Three-Vessel Global Ischemia Model in Rat

Neurodegeneration, Myelin Loss and Glial Response in the Three-Vessel Global Ischemia Model in Rat

Effects of Fluoxetine on Hippocampal Neurogenesis and Neuroprotection in the Model of Global Cerebral Ischemia in Rats

Effect of Fluoxetine on Neurogenesis in Hippocampal Dentate Gyrus after Global Transient Cerebral Ischemia in Rats

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