Lesion of area postrema attenuated hyperphagic responses to glucoprivation, but not transcriptional activation of the neuropeptide Y gene in rats

Lesion of area postrema attenuated hyperphagic responses to glucoprivation, but not transcriptional activation of the neuropeptide Y gene in rats
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DOI:
10.1097/wnr.0b013e3283556676
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发表时间:
2012-08-01
期刊:
影响因子:
1.7
通讯作者:
Oiso, Yutaka
Oiso, Yutaka
中科院分区:
医学4区
文献类型:
--
作者:
Ozawa, Yoshiharu;Arima, Hiroshi;Oiso, Yutaka

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后区(AP)是一个缺乏血脑屏障的室周器官。先前的研究表明,AP(APX)的损伤减弱了对葡萄糖缺乏的过度进食反应。由于促食欲神经肽 Y (NPY) 神经元与食物摄入的调节有关,我们检查了糖缺乏对 NPY 神经元的激活是否也是通过 AP 介导的。与之前的研究一致,与假手术 (Sham) 组相比,APX 组对注射 2-脱氧-D-葡萄糖(阻止葡萄糖利用)的食欲亢进反应显着减弱。然而,在APX组和Sham组中注射2-脱氧-D-葡萄糖后,弓状核中NPY异核RNA(基因转录的敏感指标)的表达水平显着增加,并且各组之间的值没有显着差异。这些数据表明,对葡萄糖缺乏的贪食反应,而不是弓状核中 NPY 基因转录的激活,是通过后脑中的 AP 介导的。 NeuroReport 23:673-675 (C) 2012 Wolters Kluwer Health 垂直条 Lippincott Williams & Wilkins。
The area postrema (AP) is a circumventricular organ that lacks a blood-brain barrier. Previous studies have shown that the lesion of AP (APX) attenuated hyperphagic responses to glucoprivation. As the orexigenic neuropeptide Y (NPY) neurons have been implicated in the regulation of food intake, we examined whether the activation of NPY neurons by glucoprivation is mediated through the AP as well. In agreement with previous studies, hyperphagic responses to an injection of 2-deoxy-D-glucose that blocks glucose utilization were significantly attenuated in the APX group compared with the sham-operated (Sham) group. However, the expression levels of NPY heteronuclear RNA, a sensitive indicator for the gene transcription, were significantly increased in the arcuate nucleus by a 2-deoxy-D-glucose injection in both the APX and the Sham groups, and there were no significant differences in the values between groups. These data suggest that the hyperphagic response to glucoprivation, but not the activation of NPY gene transcription in the arcuate nucleus, was mediated through the AP in the hindbrain. NeuroReport 23:673-675 (C) 2012 Wolters Kluwer Health vertical bar Lippincott Williams & Wilkins.