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实验性糖尿病发展的前两周内海马结构的重塑。

Remodeling of ammon's horn during the first two weeks of experimental diabetes development.

作者信息

Lebed Y V, Orlovsky M A, Tsupikov O M, Pivneva T A, Skibo G G

机构信息

O. O. Bogomoletz Institute of Physiology, National Academy of Sciences of Ukraine, Kyiv.

出版信息

Fiziol Zh (1994). 2008;54(3):52-6.

PMID:18763580
Abstract

It is known that long-term diabetes mellitus causes hippocampal dysfunction, however, early events leading to diabetes-related impairments of hippocampal tissue remain obscure. The present study was performed to examine temporal and spatial patterns of neuronal damage and astrogliosis in hippocampal CA1-C3 areas during the early stage of streptozotocin-induced diabetes in rats. NeuN and GFAP immunohistochemistry was used to visualize neurons and glial cells. Immunopositive cells were counted in hippocampal CA1-CA3 areas at days 3, 7 and 14 of diabetes development using confocal Olympus FV1000 microscope. Significant decrease in the number of neurons in CA2 area was observed in diabetic rats at day 3. In contrast, in CA1 and CA3 areas NeuN-positive cell count started to decrease later being at day 7, correspondingly, by 7 and 9 % lower than that in the control. This trend developed further till day 14, when the number of neurons in CA1 and CA3 areas was, respectively, 20.3 and 18.1% smaller as compared with the control. These changes were accompanied by astrogliosis: the number of astrocytes in pyramidal cell layer was increased significantly in all examined time-points. Thus, our study demonstrates that streptozotocin-induced diabetes is associated with early neurodegeneration in Ammon's horn. It suggests that clinically relevant cognitive deficits development in diabetic patients starting from the early stage of the disease.

摘要

已知长期糖尿病会导致海马功能障碍,然而,导致糖尿病相关海马组织损伤的早期事件仍不清楚。本研究旨在检查链脲佐菌素诱导的糖尿病大鼠早期海马CA1 - C3区神经元损伤和星形胶质细胞增生的时间和空间模式。使用NeuN和GFAP免疫组织化学来观察神经元和胶质细胞。在糖尿病发展的第3、7和14天,使用共聚焦奥林巴斯FV1000显微镜对海马CA1 - CA3区的免疫阳性细胞进行计数。在糖尿病大鼠的第3天,观察到CA2区神经元数量显著减少。相比之下,在CA1和CA3区,NeuN阳性细胞计数在第7天开始下降,分别比对照组低7%和9%。这种趋势一直持续到第14天,此时CA1和CA3区的神经元数量分别比对照组少20.3%和18.1%。这些变化伴随着星形胶质细胞增生:在所有检查的时间点,锥体细胞层中的星形胶质细胞数量显著增加。因此,我们的研究表明,链脲佐菌素诱导的糖尿病与海马角早期神经退行性变有关。这表明糖尿病患者从疾病早期就开始出现临床上相关的认知缺陷。

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