POTENTIATION OF CCK-8 ON FOOD INTAKE BY ESTRADIOL

性腺类固醇是影响食物摄入量的众多因素之一。 以及大鼠的体重。荷尔蒙对这些过程的影响是 在女性中尤其引人注目，她们的食物数量大幅增加 卵巢切除后的摄入量和体重。这些变化是可以逆转的 通过外周用雌二醇治疗或通过直接放置 下丘脑室旁核(PVN)内的雌二醇(E_2)。 尽管人们认识到雌二醇对摄食的影响需要 荷尔蒙在大脑中的作用，E2通过的神经机制 抑制食物摄入量仍有待具体说明。外周注射 荷尔蒙CCK(CCK)在许多情况下减少食物摄入量 物种，CCK现在被视为一种重要的生理信号 饱腹感。已有研究表明，操纵卵巢激素可以改变CCK 包括下丘脑室旁核在内的几个下丘脑核团的活动表明 雌激素对摄食的影响可能是通过调节 大脑中的CCK系统。按照这些思路，最近的情况是 研究表明，外周使用雌二醇组可增强 腹腔注射CCK对雌性大鼠摄食量的影响。这个 拟议中的实验将尝试证实和扩展这一现象 通过确定E2作用于大脑的哪个部位来增加饱腹感 CCK的作用以及通过检测中枢CCK受体所起的作用 在类固醇和多肽的相互作用中。据推测，雌二醇可增强 下丘脑室旁核中的CCK活性，进而加强CCK对食物的影响 摄取和调节E2对进食的抑制作用。第一 实验将评估这一假说，将中央植入 稀释下丘脑室旁核、下丘脑腹内侧核(VMN)和 雌性大鼠视前区(POA)。它还假设， 雌激素增强CCK的饱足效应需要刺激 下丘脑室旁核中CCK的大脑受体。第二个实验将 2种不同CCK受体的PVN输注效果观察 拮抗剂对单独由E2、CCK产生的摄食抑制作用 单用E_2和CCK联合治疗。获取的信息 这些实验将有助于我们了解大脑 摄食行为的机制和类固醇的作用方式 荷尔蒙会影响大脑功能。

Gonadal steroids are among the numerous factors influencing food intake and body weight in rats. Hormonal effects on these processes are particularly striking in females, which show large increases in food intake and body weight after ovariectomy. These changes can be reversed by peripheral treatment with estradiol or by direct placement of estradiol (E2) in the hypothalamic paraventricular nucleus (PVN). Although it is acknowledged that the effects of E2 on feeding require actions of the hormone within the brain, the neural mechanism by which E2 suppresses food intake remains to be specified. Peripheral injections of the hormone cholecystokinin (CCK) reduce food intake in a number of species, and CCK is now viewed as an important physiological signal for satiety. Manipulation of ovarian hormones has been shown to alter CCK activity in several hypothalamic nuclei, including the PVN, suggesting that the effects of E2 on feeding may be mediated by the modulation of CCK systems within the brain. Along these lines, it has recently been shown that peripheral treatment with E2 potentiates the effects of intraperitoneal (ip) injections of CCK on food intake in female rats. The proposed experiments will attempt to confirm and extend this phenomenon by identifying the brain site at which E2 acts to augment the satiety effect of CCK, and by examining the role played by central CCK receptors in this steroid-peptide interaction. It is hypothesized that E2 enhances CCK activity in the PVN , which in turn potentiates CCK's effects on food intake and mediates the suppressive effects of E2 on eating. The first experiment will evaluate this hypothesis by placing central implants of dilute E2 in the PVN, ventromedial nucleus of the hypothalamus (VMN) and preoptic area (POA)of female rats. It is also hypothesized that the potentiation of the satiety effect of CCK by E2 requires the stimulation of brain receptors for CCK in the PVN. The second experiment will examine the effects of PVN infusions of 2 different CCK receptor antagonists on the suppression of food intake produced by E2 alone, CCK alone and the combined treatment of E2 and CCK. Information obtained from these experiments will contribute to our understanding of brain mechanisms involved in feeding behavior and the ways in which steroid hormones affect brain function.