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中枢5,7-二羟基色胺对大鼠医源性下丘脑综合征的影响。

Effects of central 5,7-dihydroxytryptamine on the medical hypothalamic syndrome in rats.

作者信息

Coscina D V

出版信息

Ann N Y Acad Sci. 1978 Jun 12;305:627-44. doi: 10.1111/j.1749-6632.1978.tb31553.x.

Abstract

The present study attempted to replicate and extend two recent studies that implicated aberrant brain 5-HT neurotransmission in the etiology of overeating and BW grain. Adult female rats received 25 mg/kg of desipramine hydrochloride 30--45 min prior to an intracisternal injection of 200 microgram (free base) of 5,7-DHT creatinine sulfate or its 1% ascorbic acid aqueous vehicle. After 7 weeks of measuring food intake, water intake, and BW change, rats from both groups received radiofrequency lesions of the MH or sham surgery. After 5 additional weeks of intake and BW measurements, all rats were tested for 24-hr acceptance of varying sucrose and quinine solutions and for 25-day acceptance of a high-fat replacement diet. While 5,7-DHT depleted brain 5-HT by 45%, it did not induce overeating and BW gain alone nor did it modify the overeating, obesity, or "finickiness" produced by hypothalamic injury. Several factors that relate to specificity, sufficiency, and compatibility with other 5-HT depletory techniques were discussed, as were factors of similarity and dissimilarity between this and the previous experiments that we attempted to replicate.

摘要

本研究试图重复并扩展最近的两项研究,这两项研究表明大脑5-羟色胺(5-HT)神经传递异常与暴饮暴食及体重增加的病因有关。成年雌性大鼠在脑池内注射200微克(游离碱)硫酸5,7-二羟色胺肌酐或其1%抗坏血酸水溶液前30 - 45分钟,接受25毫克/千克盐酸地昔帕明注射。在测量食物摄入量、饮水量和体重变化7周后,两组大鼠均接受内侧下丘脑(MH)的射频损伤或假手术。在额外进行5周的摄入量和体重测量后,所有大鼠都接受了为期24小时的不同蔗糖和奎宁溶液接受度测试,以及为期25天的高脂替代饮食接受度测试。虽然5,7-二羟色胺使大脑5-HT减少了45%,但它单独并不会诱发暴饮暴食和体重增加,也不会改变下丘脑损伤所导致的暴饮暴食、肥胖或“挑食”。文中讨论了与特异性、充分性以及与其他5-HT耗竭技术的兼容性相关的几个因素,以及本实验与我们试图重复的先前实验之间的异同因素。

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