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MPTP-N-氧化物使小鼠心脏去甲肾上腺素耗竭,但不影响脑内儿茶酚胺。

Depletion of cardiac norepinephrine but not brain catecholamines by MPTP-N-oxide in mice.

作者信息

Hemrick-Luecke S K, Robertson D W, Fuller R W

机构信息

Lilly Research Laboratories, Eli Lilly and Company, Indianapolis, IN 46285.

出版信息

Life Sci. 1990;47(9):815-9. doi: 10.1016/0024-3205(90)90554-5.

Abstract

After a single dose in mice, MPTP-N-oxide caused a dose-dependent depletion of cardiac norepinephrine which was similar although less pronounced than that caused by MPTP itself. After repeated daily doses, MPTP-N-oxide depleted cardiac norepinephrine, but did not deplete norepinephrine in the frontal cortex or dopamine in the striatum of mice. MPTP-N-oxide differed from MPTP, which depleted cardiac norepinephrine, cortical norepinephrine and striatal dopamine after repeated daily doses, but was similar to MPP+, another metabolite of MPTP, which depleted only cardiac norepinephrine. These data suggest that MPTP-N-oxide may contribute to the peripheral catecholamine-depleting effects after MPTP injection.

摘要

在给小鼠单次给药后,MPTP-N-氧化物导致心脏去甲肾上腺素呈剂量依赖性耗竭,这与MPTP本身引起的情况相似,尽管程度较轻。在每日重复给药后,MPTP-N-氧化物使心脏去甲肾上腺素耗竭,但未使小鼠额叶皮质中的去甲肾上腺素或纹状体中的多巴胺耗竭。MPTP-N-氧化物与MPTP不同,MPTP在每日重复给药后会使心脏去甲肾上腺素、皮质去甲肾上腺素和纹状体多巴胺耗竭,但与MPTP的另一种代谢产物MPP+相似,MPP+仅使心脏去甲肾上腺素耗竭。这些数据表明,MPTP-N-氧化物可能在MPTP注射后对外周儿茶酚胺耗竭效应起作用。

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