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Glial and neuronal dysfunction in streptozotocin-induced diabetic rats

机译:链脲佐菌素诱导的糖尿病大鼠的神经胶质和神经元功能障碍

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摘要

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.
机译:在大鼠中通过链脲佐菌素注射剂诱导糖尿病后不久就注意到神经元功能异常。从解剖学证据尚不清楚神经胶质细胞功能障碍是否伴随着有据可查的神经元缺陷。在这里,我们分离了全视野视网膜电图的Müller细胞驱动的慢速P3成分,并显示它在链脲佐菌素高血糖症发作后4周减弱。我们还发现光电导级联反应的灵敏度同时降低,以及已知可指示视网膜神经节细胞和无长蛋白细胞完整性的视网膜电图成分。我们的数据支持在链脲佐菌素诱导的高血糖症中神经元和Müller细胞功能障碍同时发生的想法。

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