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[药物性帕金森综合征的发病机制(氟哌啶醇作用的实验生化及生物电研究)]

[The mechanism of the pathogenesis of drug-induced parkinsonism (experimental biochemical and bioelectrical research on the action of haloperidol)].

作者信息

Dovedova E L, Popova N S

出版信息

Zh Nevrol Psikhiatr Im S S Korsakova. 1993;93(6):15-8.

PMID:8160492
Abstract

Haloperidol was administered to rabbits in a dose 500 micrograms/kg during 60 min or 30 days. Its effects were studied in enzymes controlling neurotransmitters utilization--monoamine oxidase (MAO) A and B, acetylcholine esterase (ACE) in synaptosomes subfractions and mitochondria of the cells--and on the content of biogenic amines in the sensomotor cortex and caudate nucleus tissues. It was found that this neuroleptic induces reciprocal changes in MAO specific activity (a decrease in MAO B activity and an increase in MAO A), a fall in the levels of dopamine and noradrenaline in unchanged levels of 5'-HT and 5'-HYAA.

摘要

将氟哌啶醇以500微克/千克的剂量给兔子注射60分钟或30天。研究了其对控制神经递质利用的酶——单胺氧化酶(MAO)A和B、突触体亚组分及细胞线粒体中的乙酰胆碱酯酶(ACE)——的影响,以及对感觉运动皮层和尾状核组织中生物胺含量的影响。发现这种抗精神病药物会引起MAO比活性的相互变化(MAO B活性降低,MAO A活性增加),5'-HT和5'-HYAA水平不变的情况下多巴胺和去甲肾上腺素水平下降。

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