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参与下丘脑性食欲亢进-肥胖综合征的室旁核-后脑通路。

PVN-hindbrain pathway involved in the hypothalamic hyperphagia-obesity syndrome.

作者信息

Kirchgessner A L, Sclafani A

机构信息

Health Science Center, Brooklyn State University of New York 11203.

出版信息

Physiol Behav. 1988;42(6):517-28. doi: 10.1016/0031-9384(88)90153-9.

Abstract

This study examined the involvement of caudal brainstem projections of the hypothalamic paraventricular nucleus (PVN) in the medial hypothalamic (MH) hyperphagia-obesity syndrome. Experiment 1 demonstrated that a unilateral parasagittal knife cut in the MH combined with a contralateral coronal knife cut in either the ventrolateral pons (vP) or ventrolateral medulla (vM) significantly increased food intake and body weight in adult female rats. Overeating and overweight were also produced by a unilateral MH knife cut combined with a contralateral oblique cut under the nucleus of the solitary tract and dorsal motor nucleus of the vagus complex (NST/DX). In contrast, an MH cut x dorsolateral medullary cut combination did not increase food intake or body weight compared to a MH cut alone or sham surgery. Experiment 2 demonstrated that the hyperphagia/obesity effect of MH x vP knife cuts was comparable to that obtained with bilateral PVN lesions, but less than that produced by bilateral MH knife cuts. Bilateral vP cuts also increased body weight but the effect was less than that obtained with the other experimental treatments. Feeding the rats a high-fat diet rather than chow potentiated the hyperphagia and obesity syndromes produced by the various lesion conditions. Taken together, these findings suggest that the medial hypothalamic hyperphagia and obesity syndrome is due, in part, to damage to PVN projections to the caudal brainstem, the NST/DX complex in particular. The functional significance of this PVN-hindbrain "feeding" pathway and the identity of extra-PVN components of the hyperphagia-obesity syndrome remain to be established.

摘要

本研究考察了下丘脑室旁核(PVN)向尾侧脑干的投射在丘脑内侧(MH)摄食亢进 - 肥胖综合征中的作用。实验1表明,在MH进行单侧矢状旁切口并在腹外侧脑桥(vP)或腹外侧延髓(vM)进行对侧冠状切口,可显著增加成年雌性大鼠的食物摄入量和体重。单侧MH切口与在孤束核和迷走神经背运动核复合体(NST/DX)下方进行对侧斜切口相结合,也会导致暴饮暴食和体重增加。相比之下,与单独的MH切口或假手术相比,MH切口与背外侧延髓切口相结合并不会增加食物摄入量或体重。实验2表明,MH×vP切口产生的摄食亢进/肥胖效应与双侧PVN损伤相当,但小于双侧MH切口产生的效应。双侧vP切口也会增加体重,但效应小于其他实验处理。给大鼠喂食高脂饮食而非普通食物会增强各种损伤条件下产生的摄食亢进和肥胖综合征。综上所述,这些发现表明,丘脑内侧摄食亢进和肥胖综合征部分归因于PVN向尾侧脑干的投射受损,尤其是NST/DX复合体。这条PVN - 后脑“进食”通路的功能意义以及摄食亢进 - 肥胖综合征中PVN以外成分的身份仍有待确定。

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