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正电子发射断层扫描和磁共振成像显示猕猴脑中的锰诱导性病变

Manganese induced brain lesions in Macaca fascicularis as revealed by positron emission tomography and magnetic resonance imaging.

作者信息

Eriksson H, Tedroff J, Thuomas K A, Aquilonius S M, Hartvig P, Fasth K J, Bjurling P, Långström B, Hedström K G, Heilbronn E

机构信息

Department of Neurochemistry and Neurotoxicology, Stockholm University, Sweden.

出版信息

Arch Toxicol. 1992;66(6):403-7. doi: 10.1007/BF02035130.

DOI:10.1007/BF02035130
PMID:1444804
Abstract

A series of positron emission tomography scans was made on two monkeys during a 16-month period when they received manganese(IV)oxide by subcutaneous injection. The distribution of [11C]-nomifensine uptake, indicating dopamine terminals, was followed in both monkey brains. The brain distributions of [11C]-raclopride, demonstrating D2 dopamine receptors, and [11C]-L-dopa, as a marker of dopamine turnover, were followed in one monkey each. The monkeys developed signs of poisoning namely unsteady gait and hypoactivity. The [11C]-nomifensine uptake in the striatum was reduced with time and reached a 60% reduction after 16 months exposure. This supports the suggestion that dopaminergic nerve endings degenerate during manganese intoxication. The [11C]-L-dopa decarboxylation was not significantly altered indicating a sparing of [11C]-L-dopa decarboxylation during manganese poisoning. A transient decrease of [11C]-raclopride binding occurred but at the end of the study D2-receptor binding had returned to starting values. The magnetic resonance imaging (MRI) revealed that the manganese accumulated in the globus pallidus, putamen and caudate nucleus. There were also suggestions of gliosis/edema in the posterior limb of the internal capsule. MRI might be useful to follow manganese intoxication in humans as long as the scan is made within a few months of exposure to manganese, i.e. before a reversal of the manganese accumulation.

摘要

在16个月的时间里,对两只猴子进行了一系列正电子发射断层扫描,在此期间它们通过皮下注射接受二氧化锰。在两只猴子的大脑中追踪了指示多巴胺末梢的[11C] - 诺米芬辛摄取的分布情况。在每只猴子中分别追踪了显示D2多巴胺受体的[11C] - 雷氯必利和作为多巴胺周转标志物的[11C] - L - 多巴在大脑中的分布情况。猴子出现了中毒迹象,即步态不稳和活动减少。纹状体中[11C] - 诺米芬辛的摄取随时间减少,在暴露16个月后减少了60%。这支持了多巴胺能神经末梢在锰中毒期间退化的观点。[11C] - L - 多巴脱羧作用没有显著改变,表明在锰中毒期间[11C] - L - 多巴脱羧作用未受影响。[11C] - 雷氯必利结合出现短暂下降,但在研究结束时D2受体结合已恢复到起始值。磁共振成像(MRI)显示锰在苍白球、壳核和尾状核中蓄积。在内囊后肢也有胶质增生/水肿的迹象。只要在接触锰后的几个月内进行扫描,即锰蓄积逆转之前,MRI可能有助于追踪人类的锰中毒情况。

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