Striatal dopaminergic D1 and D2 receptors after intracerebroventricular application of alloxan and streptozocin in rat.

M Salković, I Sabolić, Z Lacković
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引用次数: 22

Abstract

Intracerebroventricular application of low, nondiabetogenic doses (500 micrograms kg-1) of alloxan and streptozocin is followed by alterations of the dopaminergic system in rat striatum. In this brain region the dopamine content significantly increased, while the density of dopaminergic D1 receptors significantly decreased seven days after the intracerebroventricular application of betacytotoxics, as compared with the control group. The density of dopaminergic D2 receptors in striatum remained unchanged. Dopaminergic D1 and D2 receptors operate through signalling mechanism of G proteins, but no changes of Gs and Gi proteins content have been found in rat striatum after the intracerebroventricular application of betacytotoxics. As intracerebroventricular, nondiabetogenic administration of betacytotoxics produces changes of the striatal dopamine content and D1 receptor density similar to that produced by peripheral, diabetogenic administration of these drugs, the effect might be related not solely to pancreatic beta cells damage, but to alterations of the brain insulin system, as well.

大鼠脑室内应用四氧嘧啶和链脲佐菌素后纹状体多巴胺能D1和D2受体。
在脑室内应用低剂量(500微克公斤-1)的四氧嘧啶和链脲菌素后,大鼠纹状体多巴胺能系统发生改变。与对照组相比,在脑室内应用β细胞毒素7天后,该脑区多巴胺含量显著增加,而多巴胺能D1受体密度显著降低。纹状体多巴胺能D2受体密度保持不变。多巴胺能D1和D2受体通过G蛋白的信号机制起作用,但大鼠纹状体在脑室内应用β细胞毒素后未发现Gs和Gi蛋白含量的变化。由于脑室内非糖尿病性给药β细胞毒素引起纹状体多巴胺含量和D1受体密度的变化与外周糖尿病性给药相似,这种影响可能不仅与胰腺β细胞损伤有关,还与脑胰岛素系统的改变有关。
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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