Involvement of prolactin-releasing peptide in the activation of oxytocin neurones in response to food intake.

Involvement of prolactin-releasing peptide in the activation of oxytocin neurones in response to food intake.
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DOI:
10.1111/jne.12019
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发表时间:
2013-05
影响因子:
3.2
通讯作者:
Onaka T
Onaka T
中科院分区:
医学3区
文献类型:
--
作者:
Yamashita M;Takayanagi Y;Yoshida M;Nishimori K;Kusama M;Onaka T

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食物摄入激活延髓中表达催乳素释放肽(PrRP)的神经元和下丘脑中的催产素神经元。PrRP和催产素都被证明具有抗抑郁作用。在本研究中,我们调查是否催产素神经元的激活后的食物摄入量介导的PrRP。我们首先检查了大鼠中PrRP受体(也称为GPR 10)的表达。PrRP受体的免疫反应性观察催产素神经元和加压素神经元的室旁核和视上核的下丘脑和床核的终纹。PrRP应用于孤立的视上核促进催产素和加压素的释放。在小鼠中,再喂养增加Fos蛋白在下丘脑和终纹床核的催产素神经元的表达。在PrRP缺陷小鼠中,再喂食或腹腔注射八肽胆囊收缩素(CCK)(一种外周饱腹感因子)后催产素神经元中Fos蛋白表达的增加受到损害。CCK诱导的血浆催产素增加也受损PrRP缺陷小鼠。此外,催产素受体缺陷小鼠表现出增加的膳食量,如PrRP缺陷小鼠和CCKA受体缺陷小鼠所报告的。这些研究结果表明,PrRP介导,至少在部分,催产素神经元的激活,在响应食物的摄入量,和CCK-PrRP-催产素通路起着重要的作用,在控制终止每餐。
Food intake activates neurones expressing prolactin-releasing peptide (PrRP) in the medulla oblongata and oxytocin neurones in the hypothalamus. Both PrRP and oxytocin have been shown to have an anorexic action. In the present study, we investigated whether the activation of oxytocin neurones following food intake is mediated by PrRP. We first examined the expression of PrRP receptors (also known as GPR10) in rats. Immunoreactivity of PrRP receptors was observed in oxytocin neurones and in vasopressin neurones in the paraventricular and supraoptic nuclei of the hypothalamus and in the bed nucleus of the stria terminalis. Application of PrRP to isolated supraoptic nuclei facilitated the release of oxytocin and vasopressin. In mice, re-feeding increased the expression of Fos protein in oxytocin neurones of the hypothalamus and bed nucleus of the stria terminalis. The increased expression of Fos protein in oxytocin neurones following re-feeding or i.p. administration of cholecystokinin octapeptide (CCK), a peripheral satiety factor, was impaired in PrRP-deficient mice. CCK-induced oxytocin increase in plasma was also impaired in PrRP-deficient mice. Furthermore, oxytocin receptor-deficient mice showed an increased meal size, as reported in PrRP-deficient mice and in CCKA receptor-deficient mice. These findings suggest that PrRP mediates, at least in part, the activation of oxytocin neurones in response to food intake, and that the CCK–PrRP–oxytocin pathway plays an important role in the control of the termination of each meal.
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