Glial and neuronal dysfunction in streptozotocin-induced diabetic rats.

Vickie H Y Wong, Algis J Vingrys, Bang V Bui
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引用次数: 13

Abstract

Neuronal dysfunction has been noted very soon after the induction of diabetes by streptozotocin injection in rats. It is not clear from anatomical evidence whether glial cell dysfunction accompanies the well-documented neuronal deficit. Here, we isolate the Müller cell driven slow-P3 component of the full-field electroretinogram and show that it is attenuated at 4 weeks following the onset of streptozotocin-hyperglycaemia. We also found a concurrent reduction in the sensitivity of the phototransduction cascade, as well as in the components of the electroretinogram known to indicate retinal ganglion cell and amacrine cell integrity. Our data support the idea that neuronal and Müller cell dysfunction occurs at the same time in streptozotocin-induced hyperglycaemia.

链脲佐菌素诱导的糖尿病大鼠神经胶质功能障碍。
链脲佐菌素诱导大鼠糖尿病后很快出现神经功能障碍。从解剖学证据来看,尚不清楚胶质细胞功能障碍是否伴随有文献记载的神经元缺陷。在这里,我们分离了全视野视网膜电图中由m ller细胞驱动的慢p3成分,并显示它在链脲佐菌素高血糖发作后4周减弱。我们还发现光导级联的敏感性同时降低,以及视网膜电图中已知指示视网膜神经节细胞和无突细胞完整性的成分也同时降低。我们的数据支持这样一种观点,即在链脲佐菌素诱导的高血糖中,神经元和突触细胞功能障碍同时发生。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
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