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通过中脑5-羟色胺耗竭性损伤对大鼠下丘脑性食欲亢进和肥胖进行选择性阻断。

Selective blockade of hypothalamic hyperphagia and obesity in rats by serotonin-depleting midbrain lesions.

作者信息

Coscina D V, Stancer H C

出版信息

Science. 1977 Jan 28;195(4276):416-9. doi: 10.1126/science.831288.

Abstract

Adult female rats, depleted of 70 percent of forebrain serotonin by dorsal and median raphe lesions, showed little overeating of food pellets and obesity following medial hypothalamic lesions. However, these rats showed the same reduced acceptance of sucrose solutions, enhanced rejection of quinine solutions, and exaggerated weight gain on a high-fat diet as did other rats made obese by medial hypothalamic lesions alone. Since raphe lesions alone produced none of these effects, the pattern of behaviors observed suggests a hitherto unknown (perhaps secondary) role for brain serotonin metabolism in selective aspects of the medial hypothalamic syndrome.

摘要

成年雌性大鼠通过中缝背核和中缝正中核损伤使其前脑5-羟色胺减少70%,在内侧下丘脑损伤后,其对食丸的过度进食和肥胖现象并不明显。然而,这些大鼠与仅通过内侧下丘脑损伤而致肥胖的其他大鼠一样,对蔗糖溶液的接受度降低,对奎宁溶液的排斥增强,并且在高脂饮食时体重增加幅度更大。由于仅中缝核损伤不会产生这些效应,所观察到的行为模式表明,脑5-羟色胺代谢在内侧下丘脑综合征的某些选择性方面具有迄今未知(可能是继发性)的作用。

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