Exposure of experimental animals to the mitochondrial toxin rotenone is considered to be a model of environmental progression of Parkinson's disease (PD). We investigated the differential vulnerability of various brain regions to generalized inhibition of complex I, induced by subcutaneous rotenone injections for the duration of 1, 3 and 7 days in both rats (2 mg/kg dosage) and mice (4 mg/kg dosage). To examine patterns of metabolic activity changes in the brain, histochemical evaluation of cytochrome C oxidase (COX) activity was performed in post mortem brain sections. Animals displayed a similar time course of neuronal loss in substantia nigra pars compacta (SNpc), reaching 44 % in mice and 42 % in rats by the 7th day. The pattern of COX activity changes, however, was different for the two species. In both experiments, metabolic changes were evident not only in the substantia nigra, but also in non-specific structures (cortex and hippocampus). In mice, a decrease in COX activity was shown mostly for the non-specific areas (V1 cortex and ventral hippocampus) after the single exposure to rotenone. Data from the experiment conducted on rats demonstrated both an acute metabolic decrease in mesencephalic structures (SNpc and nucleus ruber) after a single injection of rotenone and secondary changes in cortical structures (S1 cortex and dorsal hippocampus) after chronic 7 day exposure. These changes reflect the general effect of rotenone on neuronal metabolic rate.

中文翻译：

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慢性皮下注射鱼藤酮的小鼠和大鼠大脑中COX组织化学的变化

实验动物暴露于线粒体毒素鱼藤酮被认为是帕金森病 (PD) 环境进展的​​模型。我们研究了大鼠（2 mg/kg 剂量）和小鼠（4 mg/kg 剂量）皮下注射鱼藤酮 1、3 和 7 天后，不同大脑区域对复合物 I 普遍抑制的不同脆弱性. 为了检查大脑中代谢活动变化的模式，在死后大脑切片中进行了细胞色素 C 氧化酶 (COX) 活性的组织化学评估。动物在黑质致密部 (SNpc) 中表现出类似的神经元丢失时间过程，到第 7 天时，小鼠达到 44%，大鼠达到 42%。然而，这两个物种的 COX 活性变化模式不同。在这两个实验中，代谢变化不仅在黑质中很明显，而且在非特异性结构（皮质和海马）中也很明显。在小鼠中，单次接触鱼藤酮后，COX 活性的降低主要出现在非特异性区域（V1 皮质和腹侧海马）。对大鼠进行的实验数据表明，单次注射鱼藤酮后中脑结构（SNpc 和核红素）的代谢急剧下降，以及长期暴露 7 天后皮层结构（S1 皮层和背海马体）的继发性变化。这些变化反映了鱼藤酮对神经元代谢率的一般影响。单次暴露于鱼藤酮后，COX 活性的降低主要出现在非特异性区域（V1 皮层和腹侧海马）。对大鼠进行的实验数据表明，单次注射鱼藤酮后中脑结构（SNpc 和核红素）的代谢急剧下降，以及长期暴露 7 天后皮层结构（S1 皮层和背海马体）的继发性变化。这些变化反映了鱼藤酮对神经元代谢率的一般影响。单次暴露于鱼藤酮后，COX 活性的降低主要出现在非特异性区域（V1 皮层和腹侧海马）。对大鼠进行的实验数据表明，单次注射鱼藤酮后中脑结构（SNpc 和核红素）的代谢急剧下降，以及长期暴露 7 天后皮层结构（S1 皮层和背海马体）的继发性变化。这些变化反映了鱼藤酮对神经元代谢率的一般影响。