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首页> 外文期刊>Neuropsychopharmacology >CRF|[ndash]|CRF1 Receptor System in the Central and Basolateral Nuclei of the Amygdala Differentially Mediates Excessive Eating of Palatable Food
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CRF|[ndash]|CRF1 Receptor System in the Central and Basolateral Nuclei of the Amygdala Differentially Mediates Excessive Eating of Palatable Food

机译:杏仁核中央和基底外侧核中的CRF | nRF | CRF1受体系统差异性地介导了过量食用美味食物

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摘要

Highly palatable foods and dieting are major contributing factors for the development of compulsive eating in obesity and eating disorders. We previously demonstrated that intermittent access to palatable food results in corticotropin-releasing factor-1 (CRF1) receptor antagonist-reversible behaviors, which include excessive palatable food intake, hypophagia of regular chow, and anxiety-like behavior. However, the brain areas mediating these effects are still unknown. Male Wistar rats were either fed chow continuously for 7 days/week (Chow/Chow group), or fed chow intermittently 5 days/week, followed by a sucrose, palatable diet 2 days/week (Chow/Palatable group). Following chronic diet alternation, the effects of microinfusing the CRF1 receptor antagonist R121919 (0, 0.5, 1.5?μg/side) in the central nucleus of the amygdala (CeA), the basolateral nucleus of the amygdala (BlA), or the bed nucleus of the stria terminalis (BNST) were evaluated on excessive intake of the palatable diet, chow hypophagia, and anxiety-like behavior. Furthermore, CRF immunostaining was evaluated in the brain of diet cycled rats. Intra-CeA R121919 blocked both excessive palatable food intake and anxiety-like behavior in Chow/Palatable rats, without affecting chow hypophagia. Conversely, intra-BlA R121919 reduced the chow hypophagia in Chow/Palatable rats, without affecting excessive palatable food intake or anxiety-like behavior. Intra-BNST treatment had no effect. The treatments did not modify the behavior of Chow/Chow rats. Immunohistochemistry revealed an increased number of CRF-positive cells in CeA—but not in BlA or BNST—of Chow/Palatable rats, during both withdrawal and renewed access to the palatable diet, compared with controls. These results provide functional evidence that the CRF–CRF1 receptor system in CeA and BlA has a differential role in mediating maladaptive behaviors resulting from palatable diet cycling.
机译:高度可口的食物和节食是肥胖和进食障碍中强迫性进食发展的主要因素。我们以前证明,间歇性获取可口食物会导致促肾上腺皮质激素释放因子1(CRF1)受体拮抗剂可逆行为,包括过量可口食物摄入,经常性食欲不足和焦虑样行为。然而,介导这些作用的大脑区域仍是未知的。雄性Wistar大鼠要么连续喂食7天/周(Chow / Chow组),要么间歇喂食5天/周,然后每周2天进行蔗糖可口饮食(Chow / Palatable组)。慢性饮食交替后,在杏仁核(CeA),杏仁核的基底外侧核(BlA)或床核微输注CRF1受体拮抗剂R121919(0、0.5、1.5?g /侧)对终末期纹状体(BNST)的摄入量进行了评估,评估其饮食摄入量过多,食物吞咽不足和焦虑样行为。此外,在饮食循环大鼠的大脑中评估了CRF免疫染色。 Intra-CeA R121919阻止了可口/可口大鼠的可口食物摄入过多和焦虑样行为,而不会影响食物吞咽不足。相反,BlaA R121919可以减轻Chow /可口大鼠的食物不足,而不会影响可口食物的摄入量或类似焦虑的行为。 BNST内治疗无效。这些治疗没有改变Chow / Chow大鼠的行为。免疫组织化学显示,与对照组相比,Chow /可口大鼠在CeA中(但在BlA或BNST中)CRF阳性细胞数量增加,而在戒断和重新获得可口饮食的过程中。这些结果提供了功能证据,证明CeA和BlA中的CRF–CRF1受体系统在介导可口的饮食循环所致的适应不良行为中起着不同的作用。

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