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糖尿病大鼠神经肌肉接头的病理生理学

Pathophysiology of the neuromuscular junction in diabetic rats.

作者信息

Constantini S, Schiller Y, Cohen A M, Rahamimoff R

出版信息

Isr J Med Sci. 1987 Jan-Feb;23(1-2):101-6.

PMID:3032845
Abstract

Using electrophysiological methods, we examined transport and transmission properties of the neuromuscular synapse in normal and diabetic rats. The stereospecific glucose transport system in the presynaptic nerve terminal was examined in two diabetic models and compared to the control. In both the streptozotocin (STZ) model and the Cohen model, a significant reduction was observed in the rates of glucose transport. A semiquantitative index for glucose transport, the glucose uptake factor, was 61 +/- 18% (SD) in the control group, 17 +/- 9% in the STZ group, and 15 +/- 10% in the Cohen group. Diabetes also affects the liberation of acetylcholine from the presynaptic motor nerve endings. The mean number of acetylcholine quanta liberated by the nerve impulse [quantal content (QC)] was reduced by 43% after 3.5 months of STZ diabetes. Thus, both the metabolic and the transmission functions of the neuromuscular junction are affected by the diabetic state.

摘要

我们采用电生理方法,研究了正常大鼠和糖尿病大鼠神经肌肉突触的转运和传递特性。在两种糖尿病模型中检测了突触前神经末梢的立体特异性葡萄糖转运系统,并与对照组进行比较。在链脲佐菌素(STZ)模型和科恩模型中,均观察到葡萄糖转运速率显著降低。葡萄糖转运的半定量指标——葡萄糖摄取因子,在对照组为61±18%(标准差),在STZ组为17±9%,在科恩组为15±10%。糖尿病还会影响突触前运动神经末梢乙酰胆碱的释放。在STZ诱导糖尿病3.5个月后,神经冲动释放的乙酰胆碱量子平均数量[量子含量(QC)]降低了43%。因此,糖尿病状态会影响神经肌肉接头的代谢和传递功能。

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