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[3H]麦角吲哚与下丘脑下区域结合的调节:参与糖缺乏性摄食。

Regulation of [3H]mazindol binding to subhypothalamic areas: involvement in glucoprivic feeding.

作者信息

Angel I, Kiss A, Stivers J A, Skirboll L, Crawley J N, Paul S M

出版信息

Brain Res Bull. 1986 Dec;17(6):873-7. doi: 10.1016/0361-9230(86)90101-2.

DOI:10.1016/0361-9230(86)90101-2
PMID:3801941
Abstract

The distribution of low-affinity sodium-sensitive binding sites of [3H]mazindol were studied in rat hypothalamic nuclei. Using microdissection methods, it was demonstrated that the highest level of [3H]mazindol binding is localized to the paraventricular nucleus (PVN) and the lowest binding is observed in the lateral hypothalamus. Following food deprivation, a significant decrease in [3H]mazindol binding in the PVN and ventromedial hypothalamus (VHM) were observed. Refeeding food-deprived rats resulted in restoration of the level of binding in the PVN, and this was correlated with changes in blood glucose levels. Thus, changes in the binding of [3H]mazindol in the PVN may reflect local changes in glucose levels. In related studies, the involvement of the PVN in the regulation of food deprivation or 2-deoxyglucose (2-DG)-induced food intake was studied. Application of amphetamine (20 micrograms) into the PVN had no effect on food deprivation induced feeding, but significantly inhibited 2-DG induced (glucoprivic) feeding. The PVN may play an important role in the glucostatic regulation of feeding and in mediating the anorectic action of amphetamine and related anorectic drugs on glucoprivic feeding.

摘要

研究了[3H]马吲哚低亲和力钠敏感结合位点在大鼠下丘脑核团中的分布。采用显微解剖方法表明,[3H]马吲哚结合水平最高的区域位于室旁核(PVN),而在下丘脑外侧观察到的结合水平最低。禁食后,观察到PVN和腹内侧下丘脑(VHM)中[3H]马吲哚结合显著减少。给禁食大鼠重新喂食导致PVN中结合水平恢复,这与血糖水平变化相关。因此,PVN中[3H]马吲哚结合的变化可能反映了局部葡萄糖水平的变化。在相关研究中,研究了PVN在禁食或2-脱氧葡萄糖(2-DG)诱导的食物摄入调节中的作用。向PVN注射苯丙胺(20微克)对禁食诱导的进食没有影响,但显著抑制2-DG诱导的(糖缺乏性)进食。PVN可能在进食的糖稳态调节以及介导苯丙胺和相关厌食药物对糖缺乏性进食的厌食作用中发挥重要作用。

相似文献

1
Regulation of [3H]mazindol binding to subhypothalamic areas: involvement in glucoprivic feeding.[3H]麦角吲哚与下丘脑下区域结合的调节:参与糖缺乏性摄食。
Brain Res Bull. 1986 Dec;17(6):873-7. doi: 10.1016/0361-9230(86)90101-2.
2
Site of action of anorectic drugs: glucoprivic- versus food deprivation-induced feeding.食欲抑制药物的作用部位:糖缺乏与食物剥夺诱导的进食
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Glucose regulates [3H](+)-amphetamine binding and Na+K+ ATPase activity in the hypothalamus: a proposed mechanism for the glucostatic control of feeding and satiety.葡萄糖调节下丘脑的[3H](+)-苯丙胺结合及钠钾ATP酶活性:一种关于进食和饱腹感的葡萄糖稳态控制的潜在机制。
Brain Res Bull. 1986 Feb;16(2):281-8. doi: 10.1016/0361-9230(86)90043-2.

引用本文的文献

1
Proceedings of the British Pharmacological Society. 6th-8th January, 1988. Abstracts.英国药理学会会议记录。1988年1月6日至8日。摘要
Br J Pharmacol. 1988 Mar;93 Suppl(Suppl):1P-311P.