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苯丙胺诱导的乙醇摄入量增加:中枢儿茶酚胺的作用

Amphetamine-induced enhancement of ethanol consumption: role of central catecholamines.

作者信息

Levy A D, Ellison G

出版信息

Psychopharmacology (Berl). 1985;86(1-2):233-6. doi: 10.1007/BF00431716.

Abstract

Rats administered continuous low levels of amphetamine increase their free choice consumption of a 10% ethanol solution. The present experiment sought to determine the roles of central catecholamines in producing this effect by comparing the changes of ethanol consumption in rats implanted with control pellets or amphetamine pellets following intracerebral injections of 2 X 250 micrograms of 6-hydroxydopamine (6-OHDA), 6-OHDA preceded by 25 mg/kg of desipramine (to protect noradrenergic neurons from damage), or vehicle. The increase of ethanol consumption associated with continuous amphetamine administration was prevented by intracerebral 6-OHDA administration, but not by intracerebral 6-OHDA preceded by desipramine. There were no significant changes of ethanol consumption in animals receiving either 6-OHDA regimen followed by control pellet implantation. These data indicate that the increased consumption of ethanol obtained with continuous amphetamine administration is mediated by central noradrenergic systems.

摘要

持续给予低剂量苯丙胺的大鼠会增加其对10%乙醇溶液的自由选择摄入量。本实验旨在通过比较脑内注射2×250微克6-羟基多巴胺(6-OHDA)、注射25毫克/千克地昔帕明(以保护去甲肾上腺素能神经元免受损伤)后再注射6-OHDA或注射溶剂后,植入对照丸剂或苯丙胺丸剂的大鼠乙醇摄入量的变化,来确定中枢儿茶酚胺在产生这种效应中的作用。脑内注射6-OHDA可阻止与持续给予苯丙胺相关的乙醇摄入量增加,但在注射地昔帕明后再注射6-OHDA则无此效果。接受两种6-OHDA给药方案后再植入对照丸剂的动物,其乙醇摄入量无显著变化。这些数据表明,持续给予苯丙胺导致的乙醇摄入量增加是由中枢去甲肾上腺素能系统介导的。

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