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Impaired Satiation and Increased Feeding Behaviour in the Triple-Transgenic Alzheimers Disease Mouse Model

机译:受损饱食而在三转基因阿尔茨海默氏症小鼠模型增加摄食行为

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摘要

Alzheimer's disease (AD) is associated with non-cognitive symptoms such as changes in feeding behaviour that are often characterised by an increase in appetite. Increased food intake is observed in several mouse models of AD including the triple transgenic (3×TgAD) mouse, but the mechanisms underlying this hyperphagia are unknown. We therefore examined feeding behaviour in 3×TgAD mice and tested their sensitivity to exogenous and endogenous satiety factors by assessing food intake and activation of key brain regions. In the behavioural satiety sequence (BSS), 3×TgAD mice consumed more food after a fast compared to Non-Tg controls. Feeding and drinking behaviours were increased and rest decreased in 3×TgAD mice, but the overall sequence of behaviours in the BSS was maintained. Exogenous administration of the satiety factor cholecystokinin (CCK; 8–30 µg/kg, i.p.) dose-dependently reduced food intake in Non-Tg controls and increased inactive behaviour, but had no effect on food intake or behaviour in 3×TgAD mice. CCK (15 µg/kg, i.p.) increased c-Fos protein expression in the supraoptic nucleus of the hypothalamus, and the nucleus tractus solitarius (NTS) and area postrema of the brainstem to the same extent in Non-Tg and 3×TgAD mice, but less c-Fos positive cells were detected in the paraventricular hypothalamic nucleus of CCK-treated 3×TgAD compared to Non-Tg mice. In response to a fast or a period of re-feeding, there was no difference in the number of c-Fos-positive cells detected in the arcuate nucleus of the hypothalamus, NTS and area postrema of 3×TgAD compared to Non-Tg mice. The degree of c-Fos expression in the NTS was positively correlated to food intake in Non-Tg mice, however, this relationship was absent in 3×TgAD mice. These data demonstrate that 3×TgAD mice show increased feeding behaviour and insensitivity to satiation, which is possibly due to defective gut-brain signalling in response to endogenous satiety factors released by food ingestion.
机译:阿尔茨海默氏病(AD)与非认知症状(如进食行为改变)有关,通常以食欲增加为特征。在包括三重转基因(3xTgAD)小鼠在内的几种AD小鼠模型中均观察到食物摄入增加,但这种食欲过剩的潜在机制尚不清楚。因此,我们检查了3xTgAD小鼠的进食行为,并通过评估食物摄入量和关键脑区的激活程度来测试它们对外源和内源饱足感的敏感性。在行为饱足感序列(BSS)中,与非Tg对照相比,3xTgAD小鼠在禁食后消耗了更多的食物。 3xTgAD小鼠的进食和饮水行为增加而休息减少,但在BSS中行为的总体顺序得以维持。饱足性因子胆囊收缩素(CCK; 8–30 µg / kg,腹腔注射)的外源给药在非Tg对照中剂量依赖性地减少了食物摄入并增加了非活动行为,但对3xTgAD小鼠的食物摄入或行为没有影响。在非Tg和3xTgAD小鼠中,CCK(15 µg / kg,ip)在下丘脑的视上核,孤束核(NTS)和脑干后区域增加了c-Fos蛋白表达。 ,但与非Tg小鼠相比,经CCK处理的3xTgAD的室下丘脑旁核中检测到的c-Fos阳性细胞更少。响应快速或一段时间的补饲,与非Tg小鼠相比,在下丘脑弓状核,NTS和3×TgAD的术后区域中检测到的c-Fos阳性细胞数量没有差异。 NTS中c-Fos表达的程度与非Tg小鼠的摄食量呈正相关,但是,这种关系在3xTgAD小鼠中不存在。这些数据表明3xTgAD小鼠显示出增加的进食行为和对饱足感的不敏感性,这可能是由于响应于食物摄入释放的内源饱腹感因子导致的肠脑信号缺陷所致。

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