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发作性睡病:动物模型中的生物胺缺乏

Narcolepsy: biogenic amine deficits in an animal model.

作者信息

Mefford I N, Baker T L, Boehme R, Foutz A S, Ciaranello R D, Barchas J D, Dement W C

出版信息

Science. 1983 May 6;220(4597):629-32. doi: 10.1126/science.6188216.

Abstract

Concentrations of biogenic amine metabolites in discrete brain areas differed significantly between dogs with genetically transmitted narcolepsy and age- and breed-matched controls. Dopamine and 3,4-dihydroxyphenylacetic acid were consistently elevated in the brains of narcoleptic animals, while homovanillic acid was not. Narcoleptic animals consistently exhibited lower utilization of dopamine and higher intraneuronal degradation of dopamine but no uniform decrease in serotonin utilization. Hence neuropathology appears to be associated with genetically transmitted canine narcolepsy. The data indicate a nonglobal depression of dopamine utilization or turnover or both.

摘要

患有遗传性发作性睡病的犬类与年龄和品种匹配的对照组相比,离散脑区中生物胺代谢物的浓度存在显著差异。发作性睡病动物大脑中的多巴胺和3,4-二羟基苯乙酸持续升高,而高香草酸则不然。发作性睡病动物始终表现出多巴胺利用率较低和多巴胺神经元内降解较高,但5-羟色胺利用率没有一致下降。因此,神经病理学似乎与遗传性犬类发作性睡病有关。数据表明多巴胺利用率或周转率或两者均存在非全局性降低。

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