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.
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DOI：
10.3390/ijms21176246
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发表时间：
2020-08-28
影响因子：
5.6
通讯作者：
Khodanovich M
中科院分区：
文献类型：
--
作者：
Anan'ina T;Kisel A;Kudabaeva M;Chernysheva G;Smolyakova V;Usov K;Krutenkova E;Plotnikov M;Khodanovich M
(1) 背景：虽然髓磷脂破坏是缺血性脑损伤的一个组成部分，但它很少成为研究主题，特别是在动物模型中。这项研究首次评估了导致海马损伤的全脑缺血（GCI）三血管模型中的髓磷脂和少突胶质细胞损失。此外，我们还研究了脱髓鞘与小胶质细胞和星形胶质细胞的变化以及海马少突胶质细胞发生之间的关系。 (2)方法：成年雄性Wistar大鼠(n=15)通过结扎脑供血大动脉或假手术完全阻断脑血流7分钟。术后10天和30天，用Fluoro-Jade C对脑切片进行神经变性染色，并进行免疫组织化学评估髓磷脂含量（MBP+占总面积的百分比）、少突胶质细胞（CNP+细胞）和神经元（NeuN+细胞）损失、神经炎症（Iba1+细胞）、星形胶质细胞增生（GFAP+细胞）和少突胶质细胞生成（NG2+细胞）； (3)结果：GCI后10天，仅在东方层和锥体层发现明显的髓磷脂和少突胶质细胞损失。到了第 30 天，这些海马层的脱髓鞘现象加剧并影响了放射基质。除了髓鞘质损伤、相应层中小胶质细胞和星形胶质细胞的激活和数量增加之外，还观察到 CA1 锥体神经元的损失以及新皮质和丘脑的神经变性。在 10 天的时间点，我们在辐射基质中观察到杆状小胶质细胞。在缺血后第 30 天，与持续的髓鞘质丧失同时，我们在脱髓鞘的海马层中发现了显着的少突胶质细胞生成； (4) 结论：我们的研究表明，GCI 模拟人类心脏骤停不仅会导致 CA1 区锥体神经元的损失，还会导致海马体相邻层的髓鞘质损失。
(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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影响因子：
6.3
作者：
BENVENISTE, H;JORGENSEN, MB;DIEMER, NH
通讯作者：
DIEMER, NH
影响因子：
3.5
作者：
Dawson, MRL;Polito, A;Reynolds, R
通讯作者：
Reynolds, R
影响因子：
0.7
作者：
Khodanovich, M. Yu.;Kisel, A. A.;Plotnikov, M. B.
通讯作者：
Plotnikov, M. B.
影响因子：
0.7
作者：
Chernysheva, G. A.;Smol'yakova, V. I.;Plotnikov, M. B.
通讯作者：
Plotnikov, M. B.
DOI：
10.1007/bf01557785
发表时间：
1998-01-01
期刊：
Medical Electron Microscopy
影响因子：
--
作者：
Dohi, Kenji;Shioda, Seiji;Matsumoto, Kiyoshi
通讯作者：
Matsumoto, Kiyoshi